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human androgen independent prostate cancer cells pc3 (ATCC)

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ATCC human androgen independent prostate cancer cells pc3
IC 50 curves for MIL‐53(Al) (blue line), ADG (red line) and ADGMIL‐53 (green line) using <t>PC3</t> cell line at 48 h of treatment.

IC 50 curves for MIL‐53(Al) (blue line), ADG (red line) and ADGMIL‐53 (green line) using <t>PC3</t> cell line at 48 h of treatment.

Human Androgen Independent Prostate Cancer Cells Pc3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 14442 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 14442 article reviews

human androgen independent prostate cancer cells pc3 - by Bioz Stars, 2026-07

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1) Product Images from "Solvent‐Free Process for Preparing Metal‐Organic Framework Composites Based on Carbon‐Based Quantum Dots and Their Derivatives as Drug Delivery Systems for Andrographolide"

Article Title: Solvent‐Free Process for Preparing Metal‐Organic Framework Composites Based on Carbon‐Based Quantum Dots and Their Derivatives as Drug Delivery Systems for Andrographolide

Journal: Chemistry (Weinheim an Der Bergstrasse, Germany)

doi: 10.1002/chem.202500655

Figure Legend Snippet: IC 50 curves for MIL‐53(Al) (blue line), ADG (red line) and ADGMIL‐53 (green line) using PC3 cell line at 48 h of treatment.

Techniques Used:

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Journal: Chemistry (Weinheim an Der Bergstrasse, Germany)

Article Title: Solvent‐Free Process for Preparing Metal‐Organic Framework Composites Based on Carbon‐Based Quantum Dots and Their Derivatives as Drug Delivery Systems for Andrographolide

doi: 10.1002/chem.202500655

Figure Lengend Snippet: IC 50 curves for MIL‐53(Al) (blue line), ADG (red line) and ADGMIL‐53 (green line) using PC3 cell line at 48 h of treatment.

Article Snippet: Human androgen‐independent prostate cancer cells PC3 were purchased from American Type Culture Collection (ATCC), (Manassas, VA, USA), CRL‐1435.

Techniques:

LNCaP and PC3 cells display different inflammatory phenotype. Prostate cancer LNCaP and PC3 cells were grown for 24 h, and cell lysates were immunoblotted for NLRP3 ( A ), pro- IL-1β ( B ), mature caspase-1-p20 ( C ), phospho-p65-NF-κB or p65-NF-κB ( E ), phospho-p38-MAPK or p38-MAPK ( F ), and phospho-ERK 1/2 or ERK 1/2 ( G ). β-actin or α-tubulin were used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. LNCaP cells were used as control and assumed as 1. All histograms indicate the mean ± SD of at least n = 3 independent experiments each one tested in triplicate. ** p < 0.01, *** p < 0.001 versus LNCaP cells; ( D ) prostate cancer LNCaP and PC3 cells were grown for 24 or 48 h, and the supernatants were collected for IL-1β detection by ELISA. * p < 0.05, *** p < 0.001 versus LNCaP cells.

Journal: Biomolecules

Article Title: Natriuretic Peptides Regulate Prostate Cells Inflammatory Behavior: Potential Novel Anticancer Agents for Prostate Cancer

doi: 10.3390/biom11060794

Figure Lengend Snippet: LNCaP and PC3 cells display different inflammatory phenotype. Prostate cancer LNCaP and PC3 cells were grown for 24 h, and cell lysates were immunoblotted for NLRP3 ( A ), pro- IL-1β ( B ), mature caspase-1-p20 ( C ), phospho-p65-NF-κB or p65-NF-κB ( E ), phospho-p38-MAPK or p38-MAPK ( F ), and phospho-ERK 1/2 or ERK 1/2 ( G ). β-actin or α-tubulin were used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. LNCaP cells were used as control and assumed as 1. All histograms indicate the mean ± SD of at least n = 3 independent experiments each one tested in triplicate. ** p < 0.01, *** p < 0.001 versus LNCaP cells; ( D ) prostate cancer LNCaP and PC3 cells were grown for 24 or 48 h, and the supernatants were collected for IL-1β detection by ELISA. * p < 0.05, *** p < 0.001 versus LNCaP cells.

Article Snippet: Human androgen sensitive prostate adenocarcinoma LNCaP cells, human androgen-independent prostate cancer PC3 cells, and human non-cancerous prostatic epithelial PNT2 cells were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Control, Western Blot, Enzyme-linked Immunosorbent Assay

LNCaP and PC3 cells display different Natriuretic Peptides expression levels. Prostate cancer PC3 and LNCaP cells were grown for 24 h. Gene and protein expression were assessed for NPR-1 ( A , B ), ANP ( C , D ), and BNP ( E , F ). Gene expression was assessed by RT-PCR and values were normalized to GAPDH and presented as 2 −∆∆Ct . Relative mRNA gene abundance in PC3 cells were assumed as 1. *** p < 0.001 vs. PC3 cells. Protein expression was evaluated in total extract analyzed by Western blotting. β-actin was used as a loading control. Representative Western blots images of at least n = 3 independent experiments, each one tested in triplicate, are shown.

Journal: Biomolecules

Article Title: Natriuretic Peptides Regulate Prostate Cells Inflammatory Behavior: Potential Novel Anticancer Agents for Prostate Cancer

doi: 10.3390/biom11060794

Figure Lengend Snippet: LNCaP and PC3 cells display different Natriuretic Peptides expression levels. Prostate cancer PC3 and LNCaP cells were grown for 24 h. Gene and protein expression were assessed for NPR-1 ( A , B ), ANP ( C , D ), and BNP ( E , F ). Gene expression was assessed by RT-PCR and values were normalized to GAPDH and presented as 2 −∆∆Ct . Relative mRNA gene abundance in PC3 cells were assumed as 1. *** p < 0.001 vs. PC3 cells. Protein expression was evaluated in total extract analyzed by Western blotting. β-actin was used as a loading control. Representative Western blots images of at least n = 3 independent experiments, each one tested in triplicate, are shown.

Techniques: Expressing, Gene Expression, Reverse Transcription Polymerase Chain Reaction, Western Blot, Control

ANP and BNP counteract constitutive inflammasome activation in PC3 cells. PC3 cells were treated with ANP or BNP (1 µM) for 24 h. Cell lysates were immunoblotted for caspase-1 ( A , B ), IL-1β ( A , C , D ), ASC ( E ), AIM2 ( F ), phospho-NLRP3 (Ser295) or NLRP3 ( G – I ), phospho-p65-NF-κB or p65-NF-κB ( J ), phospho-p38-MAPK or p38-MAPK ( K ). PC3 cells were pre-incubated for 1 h with SB203580 (50 µM) and then treated with ANP or BNP (1 µM) for 24 h. Cell lysates were immunoblotted for caspase-1 ( L ). β-actin was used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. All histograms indicate the mean ± SD of at least n = 3 independent experiments, each one tested in triplicate. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. untreated PC3 cells.

Journal: Biomolecules

Article Title: Natriuretic Peptides Regulate Prostate Cells Inflammatory Behavior: Potential Novel Anticancer Agents for Prostate Cancer

doi: 10.3390/biom11060794

Figure Lengend Snippet: ANP and BNP counteract constitutive inflammasome activation in PC3 cells. PC3 cells were treated with ANP or BNP (1 µM) for 24 h. Cell lysates were immunoblotted for caspase-1 ( A , B ), IL-1β ( A , C , D ), ASC ( E ), AIM2 ( F ), phospho-NLRP3 (Ser295) or NLRP3 ( G – I ), phospho-p65-NF-κB or p65-NF-κB ( J ), phospho-p38-MAPK or p38-MAPK ( K ). PC3 cells were pre-incubated for 1 h with SB203580 (50 µM) and then treated with ANP or BNP (1 µM) for 24 h. Cell lysates were immunoblotted for caspase-1 ( L ). β-actin was used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. All histograms indicate the mean ± SD of at least n = 3 independent experiments, each one tested in triplicate. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. untreated PC3 cells.

Techniques: Activation Assay, Incubation, Control, Western Blot

ANP and BNP counteract PC3-derived EVs-induced inflammasome activation in PNT2 cells. Non-cancerous PNT2 cells were grown for 24 h. Cell lysates were immunoblotted for pro- IL-1β and mature caspase-1-p20 ( A ); NPR-1, ANP, and BNP ( B ). PNT2 cells were pre-incubated with ANP or BNP (1 µM) for 10 min and then treated with PC3-derived EVs (PC3-EVs) (100 µg/mL) for a 24 h. Cell lysate were immunoblotted for NLRP3 ( C , D ), phospho-NLRP3 (Ser295) ( C , H ), caspase-1 ( C , E ), IL-1β ( C , F , G ), phospho-ERK 1/2 or ERK 1/2 ( I ) and phospho-p38-MAPK or p38-MAPK ( J ). β-actin or α-tubulin were used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. All histograms indicate the mean ± SD of at least n = 3 independent experiments, each one tested in triplicate. ** p < 0.01, *** p < 0.001 vs. untreated PC3 cells. # p < 0.05, ### p < 0.001 vs. PC3-EVs treated PC3 cells.

Journal: Biomolecules

Article Title: Natriuretic Peptides Regulate Prostate Cells Inflammatory Behavior: Potential Novel Anticancer Agents for Prostate Cancer

doi: 10.3390/biom11060794

Figure Lengend Snippet: ANP and BNP counteract PC3-derived EVs-induced inflammasome activation in PNT2 cells. Non-cancerous PNT2 cells were grown for 24 h. Cell lysates were immunoblotted for pro- IL-1β and mature caspase-1-p20 ( A ); NPR-1, ANP, and BNP ( B ). PNT2 cells were pre-incubated with ANP or BNP (1 µM) for 10 min and then treated with PC3-derived EVs (PC3-EVs) (100 µg/mL) for a 24 h. Cell lysate were immunoblotted for NLRP3 ( C , D ), phospho-NLRP3 (Ser295) ( C , H ), caspase-1 ( C , E ), IL-1β ( C , F , G ), phospho-ERK 1/2 or ERK 1/2 ( I ) and phospho-p38-MAPK or p38-MAPK ( J ). β-actin or α-tubulin were used as a loading control. Representative Western blots images are shown. Histograms represent densitometric quantification. All histograms indicate the mean ± SD of at least n = 3 independent experiments, each one tested in triplicate. ** p < 0.01, *** p < 0.001 vs. untreated PC3 cells. # p < 0.05, ### p < 0.001 vs. PC3-EVs treated PC3 cells.

Techniques: Derivative Assay, Activation Assay, Incubation, Control, Western Blot

Overexpression of miR-183 promoted cell proliferation and invasion in prostate cancer. a Determination of miR-183 expression in prostate cancer by RT-qPCR assay, showing high expression of miR-183 in RWPE-1, LNCAP, and PC3 cells. * p < 0.05 vs. RWPE-1 cells, # p < 0.05 vs. LNCAP cells. b Determination of miR-183 expression following overexpression and inhibition of miR-183 in LNCAP and PC3 cells by RT-qPCR assay. c Cell viability examined by MTT assay. d , e Transwell assay for the detection of the effect of miR-183 on cell migration, blue indicates the migrated cells. f , g Transwell assay for the detection of the effect of miR-183 on cell invasion, blue indicates the invaded cells * p < 0.05 vs. mimic-NC group, # p < 0.05 vs. inhibitor-NC group. The miR-183-mimic group, miR-183-inhibitor group, mimic-NC group, and inhibitor-NC group referring to LNCaP or PC3 cells respectively transfected with miR-183 mimic, miR-183 inhibitor, mimic-NC, inhibitor-NC. Cell experiments were repeated three times

Journal: Cancer Cell International

Article Title: Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

doi: 10.1186/s12935-020-01686-x

Figure Lengend Snippet: Overexpression of miR-183 promoted cell proliferation and invasion in prostate cancer. a Determination of miR-183 expression in prostate cancer by RT-qPCR assay, showing high expression of miR-183 in RWPE-1, LNCAP, and PC3 cells. * p < 0.05 vs. RWPE-1 cells, # p < 0.05 vs. LNCAP cells. b Determination of miR-183 expression following overexpression and inhibition of miR-183 in LNCAP and PC3 cells by RT-qPCR assay. c Cell viability examined by MTT assay. d , e Transwell assay for the detection of the effect of miR-183 on cell migration, blue indicates the migrated cells. f , g Transwell assay for the detection of the effect of miR-183 on cell invasion, blue indicates the invaded cells * p < 0.05 vs. mimic-NC group, # p < 0.05 vs. inhibitor-NC group. The miR-183-mimic group, miR-183-inhibitor group, mimic-NC group, and inhibitor-NC group referring to LNCaP or PC3 cells respectively transfected with miR-183 mimic, miR-183 inhibitor, mimic-NC, inhibitor-NC. Cell experiments were repeated three times

Article Snippet: Normal prostate epithelial cell line RWPE-1(ATCC ® CRL-11609TM), androgen-dependent (LNCaP) and androgen-independent (PC3) human prostate cancer cell lines (ATCC ® CRL-1740TM) were obtained from ATCC (Manassas, VA, USA).

Techniques: Over Expression, Expressing, Quantitative RT-PCR, Inhibition, MTT Assay, Transwell Assay, Migration, Transfection

Journal: Cancer Cell International

Article Title: Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

doi: 10.1186/s12935-020-01686-x

Figure Lengend Snippet: miR-183 targets and negatively regulates the expression of TPM1 in prostate cancer. a Prediction of miR-183 downstream target genes, blue, red, and green indicates prediction results of miRDB, mirDIP and miRWalk database respectively, yellow indicates the top 100 significantly downregulated genes in GSE30994 profile, the region of number 5 referring the intersection of 4 data sets. b Expression of TPM1 in prostate cancer and normal tissues in GEPIA website. c The binding sites of miRNA and TPM1-3′UTR predicted by the software. d The interaction between miR-183 and TPM1 assessed by dual-luciferase reporter gene assay. e The expression of TPM1 in RWPE-1, LNCaP and PC3 cell lines measured by Western blot analysis. * p < 0.05 vs.. RWPE-1 cells, # p < 0.05 vs. LNCAP cells. f The expression of TPM1 measured by Western blot analysis. * p < 0.05 vs. mimic-NC, # p < 0.05 vs. inhibitor-NC group. The miR-183-mimic group, miR-183-inhibitor group, mimic-NC group, and inhibitor-NC group refer to LNCaP cells respectively transfected with miR-183 mimic, miR-183 inhibitor, mimic-NC, inhibitor-NC, respectively. Cell experiment was repeated three times

Techniques: Expressing, Binding Assay, Software, Luciferase, Reporter Gene Assay, Western Blot, Transfection

Exosomes derived from PC3 cells can be taken up by LNCaP cells. a Exosomes derived from PC3 cells were observed under a transmission electron microscope (× 5000). The size and morphology of vesicles were not uniform. b Detection of exosome diameter by DLS. c The expression of HSP70 and CD63 measured by Western blot analysis, the content of both proteins in exosomes higher than that in supernatant, lane 1 indicates exosome and lane 2 indicates cell. d The content of CD63 examined by flow cytometry. e The image of laser confocal microscopy. Exosomes derived from PC3 cells labeled by CFSE (green fluorescence) could be delivered into LNCAaP cells (× 400). Measurement data were expressed as mean ± standard deviation. Comparison between two groups was analyzed by unpaired t -test. Each experiment was repeated three times

Journal: Cancer Cell International

Article Title: Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

doi: 10.1186/s12935-020-01686-x

Figure Lengend Snippet: Exosomes derived from PC3 cells can be taken up by LNCaP cells. a Exosomes derived from PC3 cells were observed under a transmission electron microscope (× 5000). The size and morphology of vesicles were not uniform. b Detection of exosome diameter by DLS. c The expression of HSP70 and CD63 measured by Western blot analysis, the content of both proteins in exosomes higher than that in supernatant, lane 1 indicates exosome and lane 2 indicates cell. d The content of CD63 examined by flow cytometry. e The image of laser confocal microscopy. Exosomes derived from PC3 cells labeled by CFSE (green fluorescence) could be delivered into LNCAaP cells (× 400). Measurement data were expressed as mean ± standard deviation. Comparison between two groups was analyzed by unpaired t -test. Each experiment was repeated three times

Techniques: Derivative Assay, Transmission Assay, Microscopy, Expressing, Western Blot, Flow Cytometry, Confocal Microscopy, Labeling, Fluorescence, Standard Deviation, Comparison

PC3 cells-derived exosomal miR-183 downregulates TPM1. a The secretion of exosomes observed under an electron microscope (× 5000). b Quantification of HSP70 and CD63 in exosomes detected by Western blot. c The expression of f miR-183 and TPM1 in PC3 cells detected by RT-qPCR assay. d The expression of f miR-183 analyzed by RT-qPCR assay. e The expression of TPM1 in LNCaP cells evaluated by RT-qPCR assay. f The expression of TPM1 in LNCaP cells evaluated by Western blot assay. * p < 0.05 vs. exo-mimic-NC group, # p < 0.05 vs. exo-inhibitor-NC group. The exo-mimic-NC group, exo-miR-183-mimic group, exo-inhibitor-NC group, and miR-183-inhibitor group refer to exosome derived from PC3 cells respectively transfected with mimic-NC, exo-miR-183-mimic, inhibitor-NC and miR-183-inhibitor. The exosomes derived from the transfected PC3 cells were co-cultured with LNCAP cells Measurement data were expressed as mean ± standard deviation. Comparison between two groups was analyzed using independent sample t -test. Cell experiment was repeated three times

Journal: Cancer Cell International

Article Title: Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

doi: 10.1186/s12935-020-01686-x

Figure Lengend Snippet: PC3 cells-derived exosomal miR-183 downregulates TPM1. a The secretion of exosomes observed under an electron microscope (× 5000). b Quantification of HSP70 and CD63 in exosomes detected by Western blot. c The expression of f miR-183 and TPM1 in PC3 cells detected by RT-qPCR assay. d The expression of f miR-183 analyzed by RT-qPCR assay. e The expression of TPM1 in LNCaP cells evaluated by RT-qPCR assay. f The expression of TPM1 in LNCaP cells evaluated by Western blot assay. * p < 0.05 vs. exo-mimic-NC group, # p < 0.05 vs. exo-inhibitor-NC group. The exo-mimic-NC group, exo-miR-183-mimic group, exo-inhibitor-NC group, and miR-183-inhibitor group refer to exosome derived from PC3 cells respectively transfected with mimic-NC, exo-miR-183-mimic, inhibitor-NC and miR-183-inhibitor. The exosomes derived from the transfected PC3 cells were co-cultured with LNCAP cells Measurement data were expressed as mean ± standard deviation. Comparison between two groups was analyzed using independent sample t -test. Cell experiment was repeated three times

Techniques: Derivative Assay, Microscopy, Western Blot, Expressing, Quantitative RT-PCR, Transfection, Cell Culture, Standard Deviation, Comparison

PC3 cells-derived exosomal miR-183 promotes the development of prostate cancer through downregulation of TPM1. a Expression of TPM1 in LNCaP cells detected by Western blot analysis. b Detection for proliferation in LNCaP cells by CCK-8 assay. c , d Detection for migration and invasion in LNCaP cells by Transwell assay (× 200). * p < 0.05 vs. si-NC group, # p < 0.05 vs. oe-NC group. The oe-TPM1 group, si-TPM1 group, oe-NC group, and si-NC group refer to LNCaP cells transfected with oe-TPM1, si-TPM1 and their negative controls. The exo-miR-183-inhibitor + si-TPM1 group and exo-miR-183-inhibitor + si-NC group refer to si-TPM1 transfected-LNCaP cells co-cultured with exosome derived from PC3 cells transfected with miR-183-inhibitor and si-TPM1, The exo-miR-183-inhibitor + si-NC group refers to si-NC transfected-LNCaP cells co-cultured with exosome derived from PC3 cells transfected with miR-183-inhibitor. Measurement data were expressed as mean ± standard deviation. Comparisons among multiple groups were conducted by one-way analysis of variance (ANOVA) with Tukey’s post hoc test. Statistical analysis in relation to time-based measurements within each group was realized using repeated measurement ANOVA, followed by a Bonferroni’s post-hoc test. n = 6

Journal: Cancer Cell International

Article Title: Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

doi: 10.1186/s12935-020-01686-x

Figure Lengend Snippet: PC3 cells-derived exosomal miR-183 promotes the development of prostate cancer through downregulation of TPM1. a Expression of TPM1 in LNCaP cells detected by Western blot analysis. b Detection for proliferation in LNCaP cells by CCK-8 assay. c , d Detection for migration and invasion in LNCaP cells by Transwell assay (× 200). * p < 0.05 vs. si-NC group, # p < 0.05 vs. oe-NC group. The oe-TPM1 group, si-TPM1 group, oe-NC group, and si-NC group refer to LNCaP cells transfected with oe-TPM1, si-TPM1 and their negative controls. The exo-miR-183-inhibitor + si-TPM1 group and exo-miR-183-inhibitor + si-NC group refer to si-TPM1 transfected-LNCaP cells co-cultured with exosome derived from PC3 cells transfected with miR-183-inhibitor and si-TPM1, The exo-miR-183-inhibitor + si-NC group refers to si-NC transfected-LNCaP cells co-cultured with exosome derived from PC3 cells transfected with miR-183-inhibitor. Measurement data were expressed as mean ± standard deviation. Comparisons among multiple groups were conducted by one-way analysis of variance (ANOVA) with Tukey’s post hoc test. Statistical analysis in relation to time-based measurements within each group was realized using repeated measurement ANOVA, followed by a Bonferroni’s post-hoc test. n = 6

Techniques: Derivative Assay, Expressing, Western Blot, CCK-8 Assay, Migration, Transwell Assay, Transfection, Cell Culture, Standard Deviation

The mechanism graph of the regulatory function of exosomal miR-183 in prostate cancer. Exosomal miR-183 derived from PC3 cells facilitated prostate cancer LNCaP cell proliferation, migration, and invasion via downregulating TPM1

Journal: Cancer Cell International

Article Title: Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

doi: 10.1186/s12935-020-01686-x

Figure Lengend Snippet: The mechanism graph of the regulatory function of exosomal miR-183 in prostate cancer. Exosomal miR-183 derived from PC3 cells facilitated prostate cancer LNCaP cell proliferation, migration, and invasion via downregulating TPM1

Techniques: Derivative Assay, Migration

Cytotoxicity of curcumin and its cyclohexanone analogs on PC3 cells

Journal: Cancer Science

Article Title: Cyclohexanone curcumin analogs inhibit the progression of castration‐resistant prostate cancer in vitro and in vivo

doi: 10.1111/cas.13897

Figure Lengend Snippet: Cytotoxicity of curcumin and its cyclohexanone analogs on PC3 cells

Article Snippet: An androgen‐independent human prostate cancer cell line (PC3) was purchased from ATCC.

Techniques:

Anti‐invasion effect of curcumin and its cyclohexanone analogs on PC3 cells. For invasion assay, PC3 cells were treated with a non‐toxic concentration of curcumin, or its cyclohexanone analogs (A) or various concentrations of analogs 2A (B) or 2F (C). For migration assay, PC3 cells were treated with analogs 2A (D) and 2F (E). The invading or migrating cells were photographed under phase‐contrast microscopy and quantified by IMAGE J software. Data are represented as mean ± SD of three independent experiments. ** P < .01 and *** P < .001 vs control

Journal: Cancer Science

Article Title: Cyclohexanone curcumin analogs inhibit the progression of castration‐resistant prostate cancer in vitro and in vivo

doi: 10.1111/cas.13897

Figure Lengend Snippet: Anti‐invasion effect of curcumin and its cyclohexanone analogs on PC3 cells. For invasion assay, PC3 cells were treated with a non‐toxic concentration of curcumin, or its cyclohexanone analogs (A) or various concentrations of analogs 2A (B) or 2F (C). For migration assay, PC3 cells were treated with analogs 2A (D) and 2F (E). The invading or migrating cells were photographed under phase‐contrast microscopy and quantified by IMAGE J software. Data are represented as mean ± SD of three independent experiments. ** P < .01 and *** P < .001 vs control

Article Snippet: An androgen‐independent human prostate cancer cell line (PC3) was purchased from ATCC.

Techniques: Invasion Assay, Concentration Assay, Migration, Microscopy, Software, Control

Effect of analogs 2A and 2F on secretion (A,B) and activity (C,D) of MMP‐2 and MMP‐9 in PC3 cells. PC3 cells were incubated with increasing concentrations of analogs 2A (A) or 2F (B) for 24 h. MMP secretion in the culture medium was then determined by gelatin‐zymography. For MMP activity, slab gels containing culture medium of PC3 cells were directly incubated with various concentrations of analogs 2A (C) and 2F (B) for 16 h. Level of MMP secretion and activity was quantified by IMAGE J software. Data are represented as mean ± SD of three independent experiments. * P < 0.05, ** P <0.01 and *** P < .001 vs control

Journal: Cancer Science

Article Title: Cyclohexanone curcumin analogs inhibit the progression of castration‐resistant prostate cancer in vitro and in vivo

doi: 10.1111/cas.13897

Figure Lengend Snippet: Effect of analogs 2A and 2F on secretion (A,B) and activity (C,D) of MMP‐2 and MMP‐9 in PC3 cells. PC3 cells were incubated with increasing concentrations of analogs 2A (A) or 2F (B) for 24 h. MMP secretion in the culture medium was then determined by gelatin‐zymography. For MMP activity, slab gels containing culture medium of PC3 cells were directly incubated with various concentrations of analogs 2A (C) and 2F (B) for 16 h. Level of MMP secretion and activity was quantified by IMAGE J software. Data are represented as mean ± SD of three independent experiments. * P < 0.05, ** P <0.01 and *** P < .001 vs control

Article Snippet: An androgen‐independent human prostate cancer cell line (PC3) was purchased from ATCC.

Techniques: Activity Assay, Incubation, Zymography, Software, Control

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1) Product Images from "Solvent‐Free Process for Preparing Metal‐Organic Framework Composites Based on Carbon‐Based Quantum Dots and Their Derivatives as Drug Delivery Systems for Andrographolide"

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