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prostate cancer stem cells  (Celprogen Inc)


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    Celprogen Inc prostate cancer stem cells
    Prostate Cancer Stem Cells, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/prostate+cancer+stem+cells/Human+Prostate+Cancer+Stem+Cells/pmc12392137-24-20-52
    Average 93 stars, based on 11 article reviews
    prostate cancer stem cells - by Bioz Stars, 2026-09
    93/100 stars

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    In Vitro:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Animal Model:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Angiogenesis Assay:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Wound Healing Assay:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Migration:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Cell Cycle Assay:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Staining:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    H2O2 Assay:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Glutathione Assay:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Confocal Microscopy:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Flow Cytometry:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Western Blot:

    Article Title: Repurposing the Antidepressant Sertraline: A Systematic Scoping Review of Its Anticancer Mechanisms
    Article Snippet: Wang et al. (2019), China [ ] , Investigate whether CDC7 inhibition can induce senescence in TP53‐mutant HCC cells Identify and exploit vulnerabilities in senescent liver cancer cells to enhance therapeutic efficacy. Assess the effect of combining CDC7 inhibition with mTOR inhibition or sertraline to promote senolysis and tumor suppression , Cancer type : Liver Cell lines used : Hep3B Huh7 HepG2 SNU182 SNU398 SNU449 Huh6 SK‐Hep1 PLC/PRF/5 MHCC97H HCCLM3 Animal model : 6‐week‐old male BALB/c nude mice Subcutaneously injected with 5 × 10 6 Huh7 or MHCC97H liver cancer cells into the right posterior flank , CRISPR‐Cas9 genetic screening Clonogenic survival assay SA‐β‐gal staining Western blotting (CDC7, mTOR, apoptosis markers) Caspase‐3/7 apoptosis assay Gene set enrichment analysis Flow cytometry IF RNA sequencing mTOR signaling assays Neutral comet assay Live imaging of mitotic duration Tumor volume measurement in xenografts IHC MRI‐based tumor volume tracking , IC 50 : Not reported Animal model : Mice treated daily via oral gavage for 12–22 days with: ○ XL413 (50–100 mg/kg) to induce tumor senescence ○ AZD8055 (10–20 mg/kg) as mTOR inhibitor ○ Sertraline as a senolytic to selectively kill senescent cells post‐CDC7 inhibition Treatment continued until tumors reached ~2000 mm 3 or symptoms appeared , CDC7 inhibition selectively induced senescence in TP53‐mutant HCC cells, creating a therapeutic vulnerability A drug screen identified sertraline as a senolytic, inducing apoptosis in senescent HCC cells Sertraline acted by suppressing mTOR signaling and preventing feedback activation In vitro, the combination of CDC7 inhibition and sertraline significantly reduced HCC cell viability In vivo, this combination suppressed tumor growth and prolonged survival in xenograft models Sertraline's senolytic activity was comparable to mTOR inhibitors like AZD8055 Supports a “one‐two punch” strategy: CDC7 inhibition induces senescence, sertraline eliminates senescent cells. .. Chinnapaka et al. (2020), United States of America [ ] , To determine whether the TCTP inhibitor sertraline could target prostate cancer stem cells. To investigate the effects of sertraline on in vitro tumorigenesis and metastasis properties while also delineating its anticancer mechanism , Cancer type : Prostate Cell lines used : Celprogen (prostate cancer stem cells) PC3 DU145 LNCaP Animal model : None , Cell viability Colony formation Spheroid assay Angiogenesis assay Wound healing assay Trans well migration Apoptosis Cell cycle analysis ROS MitoSox staining Hydrogen peroxide assay Thiobarbituric acid reactive species assay Glutathione assay Confocal microscopy Flow cytometry Western blot , IC 50 : Celprogen = 25 μM PC3, DU145 & LNCaP = 10 μM at 48 h , Sertraline inhibited prostate cancer stem cell viability more potently than dihydroartemisinic Cytotoxicity blocked by NAC, GSH, catalase which confirms oxidative stress‐dependent killing Increased ROS, mitochondrial superoxide, H 2 O 2 ; induced lipid peroxidation and depleted GSH Reduced labile iron pool, potentially amplifying ROS toxicity Triggered mitochondrial dysfunction and apoptosis (increased cleaved caspase‐3, cleaved PARP‐1, pH2A.X) Induced G0 cell cycle arrest and downregulated cdc2, phospho‐Histone H3 Activated autophagy (increased LC3‐II, Beclin1, ATG5) Downregulated TCTP (total and phospho), surviving, XIAP, cIAP1 Suppressed stemness by decreasing ALDH1, CD44 and EMT markers (TCF8/ZEB1, LEF1) Disrupted F‐Actin cytoskeleton, impairing migration/invasion; inhibited colony, spheroid, and tube formation. .. Kharkar et al. (2020), India [ ] , Identify existing FDA‐approved drugs that exhibit cytotoxic effects against triple‐negative breast cancer cells, specifically MDA‐MB‐231, and evaluate their potential for drug repurposing as alternative breast cancer treatments , Cancer type : Breast Cell lines used : MDA‐MB‐231 Animal model : None , MTT assay , IC 50 : Not reported , Of the 70 drugs tested, 11 drugs demonstrated potent cytotoxicity (> 90% inhibition at 10 μM). Sertraline was among the top‐performing hits, showing 98.07% inhibition of MDA‐MB‐231 cells at 10 μM Literature review confirmed sertraline's prior anticancer activity, particularly in colorectal cancer, with IC 50 values ranging from 8 to 15 μM.

    Cell Culture:

    Article Title: Inhibition of 5-lipoxygenase downregulates stemness and kills prostate cancer stem cells by triggering apoptosis via activation of c-Jun N-terminal kinase
    Article Snippet: .. Well-characterized human tumor-derived prostate cancer stem cells (CD133 + , CD44 + , ALDH1 + , ABCG2 + , Nanog + , c-Myc + ) were purchased from Celprogen, Torrance, CA, USA [ ] and were cultured in medium provided by the supplier. .. CD133 + human cord blood stem cells were isolated by Dr. N. Varma from fresh cord blood (provided by the Henry Ford Hospital) using antibody-coated magnetic beads (Miltenyi Biotech, San Diego, CA, USA).

    Article Title: Increased Chemosensitivity via Targeting Testicular Nuclear Receptor 4 (TR4)-Oct4-Interleukin 1 Receptor Antagonist (IL1Ra) Axis in Prostate Cancer CD133 + Stem/Progenitor Cells to Battle Prostate Cancer
    Article Snippet: .. The C4-2 human PCa cells and prostate cancer stem cells (PCSCs, Celprogen (San Pedro, CA)) were cultured in the recommended media (Celprogen) and maintained at 37 °C in a humidified incubator at 5% CO 2 . .. The chemotherapeutic agents docetaxel and etoposide (LC Laboratories, Woburn, MA) were dissolved in 100% DMSO and stored at −20 °C until use. pCDNA3.3-OCT4 was purchased from Addgene (Cambridge, MA), purified, and used in transfection experiments.

    Article Title: Protein kinase C-delta inactivation inhibits the proliferation and survival of cancer stem cells in culture and in vivo
    Article Snippet: Breast cancer cell lines MCF7, Hs587T, and MDA231 were purchased from ATCC, and were propagated in 10% fetal bovine serum (Invitrogen, Grand Island, NY); Dulbecco’s Modification of Earle’s Media (Cellgro, Herndon, VA); 2 mM L-Glutamine (Invitrogen); 200 U Penicillin/ml; 200 μg Streptomycin/ml (Invitrogen). .. Human breast cancer stem cells (BCSC: CD133+, CD44+, SSEA3/4+, Oct4+, Alkaline Phosphatase+, Aldehyde Dehydrogenase+, Telomerase+), pancreatic cancer stem cells (PCSC: CD44 + , CD133 + , SSEA3/4 + , Oct4 + , Alkaline Phosphatase + , Aldehyde Dehydrogenase + , Telomerase + , and Nestin + ), and prostate cancer stem cells (PrCSC: CD44 + , CD133 + , SSEA3/4 + , Oct4 + , alkaline phosphatase + , aldehyde dehydrogenase + , and telomerase + ) were purchased from Celprogen (San Pedro, CA), and cultured using specialized media and tissue culture plastic and matrix, to preserve their CSC phenotype, according to the manufacturer’s instructions. .. Rottlerin was purchased from (EMD Biosciences, San Diego, CA).

    Isolation:

    Article Title: Peptide-targeted, stimuli-responsive polymersomes for delivering a cancer stemness inhibitor to cancer stem cell microtumors
    Article Snippet: .. [ 7 ] Prostate cancer stem cells isolated from prostate tumors displayed CD44, CD 133, SSEA3/4, and Oct4 markers ( http://www.celprogen.com ). ..



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