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hct 116 colon cancer cell line  (ATCC)


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    Structured Review

    ATCC hct 116 colon cancer cell line
    Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 <t>and</t> <t>HCT-116</t> cell lines.
    Hct 116 Colon Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 39530 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hct 116 colon cancer cell line/product/ATCC
    Average 99 stars, based on 39530 article reviews
    hct 116 colon cancer cell line - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties"

    Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

    Journal: RSC Advances

    doi: 10.1039/d5ra09325b

    Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.
    Figure Legend Snippet: Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.

    Techniques Used:

    Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.
    Figure Legend Snippet: Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.

    Techniques Used: Binding Assay



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    Inhibiting PDH, GLS1 and Hsp90 by the combination of CPI‐613+BPTES+17‐AAG gave rise to enhanced senolysis on senescent fibroblasts as well as the therapy‐induced senescent tumor cells. (A, B) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating (A) and senescent (B) BJ cells. For the dose of each compound in use, see the results 2.7 section for more details. ** p < 0.01 by Student's t ‐test. (C, D) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent lung <t>adenocarcinoma</t> <t>A549</t> cells. *** p < 0.001 by Student's t ‐test. (E, F) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent cervical carcinoma <t>HeLa</t> cells. *** p < 0.001 by Student's t ‐test. (G) The morphological changes of senescent BJ induced by IR, senescent A549 and HeLa cells induced by Dox at the indicated time of CPI‐613+BPTES+17‐AAG treatment under the light microscopy. The senescent cells without treatment were stained with SA‐β‐gal. Cells were imaged at magnification 200×. (H) The schematic summarization of our findings. The activities of TCA cycle and chaperones are reduced in DNA damage induced senescent cells. Co‐inhibiting Hsp90 and TCA cycle with 17‐AAG+CPI‐613+BPTES combination leads to enhanced selective elimination of senescent cells, hinting TCA cycle and glutaminolysis are novel and potent targets for senolysis.
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    Image Search Results


    Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.

    Journal: RSC Advances

    Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

    doi: 10.1039/d5ra09325b

    Figure Lengend Snippet: Combined histogram showing the IC 50 values of the Pd( ii ) complexes 4 and 5 against the MCF-7 and HCT-116 cell lines.

    Article Snippet: Cancer cell lines were obtained from the ATCC (Manassas, VA), MCF7 human breast cancer cell line (ATCC® HTB-22TM, USA), HCT-116 colon cancer cell line (ATCC CCL-247TM, USA) and human skin fibroblast (ATCC® PCS-201-012TM).

    Techniques:

    Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.

    Journal: RSC Advances

    Article Title: Synthesis, structural characterization and molecular docking analysis of novel β-ketoiminato palladium( ii ) complexes with anticancer properties

    doi: 10.1039/d5ra09325b

    Figure Lengend Snippet: Combined histogram displaying the binding energy scores of the Pd( ii ) complexes 4 and 5 against the KRAS-G13D, PIK3CA-H1047R and ATM-A112V targeted proteins in HCT-116.

    Article Snippet: Cancer cell lines were obtained from the ATCC (Manassas, VA), MCF7 human breast cancer cell line (ATCC® HTB-22TM, USA), HCT-116 colon cancer cell line (ATCC CCL-247TM, USA) and human skin fibroblast (ATCC® PCS-201-012TM).

    Techniques: Binding Assay

    Inhibiting PDH, GLS1 and Hsp90 by the combination of CPI‐613+BPTES+17‐AAG gave rise to enhanced senolysis on senescent fibroblasts as well as the therapy‐induced senescent tumor cells. (A, B) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating (A) and senescent (B) BJ cells. For the dose of each compound in use, see the results 2.7 section for more details. ** p < 0.01 by Student's t ‐test. (C, D) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent lung adenocarcinoma A549 cells. *** p < 0.001 by Student's t ‐test. (E, F) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent cervical carcinoma HeLa cells. *** p < 0.001 by Student's t ‐test. (G) The morphological changes of senescent BJ induced by IR, senescent A549 and HeLa cells induced by Dox at the indicated time of CPI‐613+BPTES+17‐AAG treatment under the light microscopy. The senescent cells without treatment were stained with SA‐β‐gal. Cells were imaged at magnification 200×. (H) The schematic summarization of our findings. The activities of TCA cycle and chaperones are reduced in DNA damage induced senescent cells. Co‐inhibiting Hsp90 and TCA cycle with 17‐AAG+CPI‐613+BPTES combination leads to enhanced selective elimination of senescent cells, hinting TCA cycle and glutaminolysis are novel and potent targets for senolysis.

    Journal: Aging Cell

    Article Title: Decreased Glucose Metabolism and Declined Chaperones Are Unique Features Required for the Survival of Senescent Fibroblasts and Pyruvate Dehydrogenase Is a Potent Senolytic Target

    doi: 10.1111/acel.70434

    Figure Lengend Snippet: Inhibiting PDH, GLS1 and Hsp90 by the combination of CPI‐613+BPTES+17‐AAG gave rise to enhanced senolysis on senescent fibroblasts as well as the therapy‐induced senescent tumor cells. (A, B) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating (A) and senescent (B) BJ cells. For the dose of each compound in use, see the results 2.7 section for more details. ** p < 0.01 by Student's t ‐test. (C, D) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent lung adenocarcinoma A549 cells. *** p < 0.001 by Student's t ‐test. (E, F) The effects of CPI‐613+BPTES+17‐AAG combination treatment on proliferating and Dox‐induced senescent cervical carcinoma HeLa cells. *** p < 0.001 by Student's t ‐test. (G) The morphological changes of senescent BJ induced by IR, senescent A549 and HeLa cells induced by Dox at the indicated time of CPI‐613+BPTES+17‐AAG treatment under the light microscopy. The senescent cells without treatment were stained with SA‐β‐gal. Cells were imaged at magnification 200×. (H) The schematic summarization of our findings. The activities of TCA cycle and chaperones are reduced in DNA damage induced senescent cells. Co‐inhibiting Hsp90 and TCA cycle with 17‐AAG+CPI‐613+BPTES combination leads to enhanced selective elimination of senescent cells, hinting TCA cycle and glutaminolysis are novel and potent targets for senolysis.

    Article Snippet: Human fibroblasts BJ (RRID: CVCL_3653; ATCC Cat#CRL‐2522), IMR‐90 (RRID: CVCL_0347; ATCC Cat#CCL‐186), WI‐38 (RRID: CVCL_0579; ATCC Cat#CCL‐75) and human cancer cell lines HeLa (RRID: CVCL_0030; ATCC Cat#CRM‐CCL‐2), A549 (RRID: CVCL_0023; ATCC Cat#CRM‐CCL‐185), and U2OS (RRID: CVCL_0042; ATCC Cat#HTB‐96) were purchased from American Type Culture Collection (ATCC) and cultured in Dulbecco's modified Eagle's medium (DMEM, Gibco) supplemented with 10% fetal bovine serum (FBS, Invitrogen) and 1% penicillin/streptomycin at 37°C under 5% CO 2 .

    Techniques: Light Microscopy, Staining

    Distinct proteomic and transcriptional signatures of metabolic enzymes and chaperones between senescent fibroblasts and the therapy‐induced senescent tumor cells. (A) The abundance of glycolysis‐related enzymes PFKP, ALDOA, PKM2, TCA cycle‐related PDHA, and glutaminolysis‐related GLS1 was decreased significantly in senescent BJ and IMR‐90 cells compared to their proliferating counterparts. (B) The protein levels of chaperones TCP1, Hsp70, and Hsp90 were decreased significantly in senescent BJ and IMR‐90 cells. (C) The abundance of those glycolysis‐related enzymes remained unchanged or even elevated in Dox‐induced senescent A549, HeLa, and U2OS tumor cells compared to their proliferating counterparts. (D) The abundance of these chaperone proteins in Dox‐induced senescent A549, HeLa, and U2OS tumor cells remained nearly unchanged. The relative abundance of each protein was quantified by signal density scanning on Western blots and normalized to the signal of β‐Actin or β‐tubulin. * p < 0.05, ** p < 0.01 tested by Student's t ‐test.

    Journal: Aging Cell

    Article Title: Decreased Glucose Metabolism and Declined Chaperones Are Unique Features Required for the Survival of Senescent Fibroblasts and Pyruvate Dehydrogenase Is a Potent Senolytic Target

    doi: 10.1111/acel.70434

    Figure Lengend Snippet: Distinct proteomic and transcriptional signatures of metabolic enzymes and chaperones between senescent fibroblasts and the therapy‐induced senescent tumor cells. (A) The abundance of glycolysis‐related enzymes PFKP, ALDOA, PKM2, TCA cycle‐related PDHA, and glutaminolysis‐related GLS1 was decreased significantly in senescent BJ and IMR‐90 cells compared to their proliferating counterparts. (B) The protein levels of chaperones TCP1, Hsp70, and Hsp90 were decreased significantly in senescent BJ and IMR‐90 cells. (C) The abundance of those glycolysis‐related enzymes remained unchanged or even elevated in Dox‐induced senescent A549, HeLa, and U2OS tumor cells compared to their proliferating counterparts. (D) The abundance of these chaperone proteins in Dox‐induced senescent A549, HeLa, and U2OS tumor cells remained nearly unchanged. The relative abundance of each protein was quantified by signal density scanning on Western blots and normalized to the signal of β‐Actin or β‐tubulin. * p < 0.05, ** p < 0.01 tested by Student's t ‐test.

    Article Snippet: Human fibroblasts BJ (RRID: CVCL_3653; ATCC Cat#CRL‐2522), IMR‐90 (RRID: CVCL_0347; ATCC Cat#CCL‐186), WI‐38 (RRID: CVCL_0579; ATCC Cat#CCL‐75) and human cancer cell lines HeLa (RRID: CVCL_0030; ATCC Cat#CRM‐CCL‐2), A549 (RRID: CVCL_0023; ATCC Cat#CRM‐CCL‐185), and U2OS (RRID: CVCL_0042; ATCC Cat#HTB‐96) were purchased from American Type Culture Collection (ATCC) and cultured in Dulbecco's modified Eagle's medium (DMEM, Gibco) supplemented with 10% fetal bovine serum (FBS, Invitrogen) and 1% penicillin/streptomycin at 37°C under 5% CO 2 .

    Techniques: Western Blot