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ATCC pc3 prostate tumour cells

Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of <t>PC3</t> cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Pc3 Prostate Tumour Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 15756 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype"

Article Title: Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype

Journal: Journal of Bone Oncology

doi: 10.1016/j.jbo.2026.100754

Figure Legend Snippet: Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Techniques Used: Co-Culture Assay, Control, Isolation, Cell Characterization

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Journal: Journal of Bone Oncology

Article Title: Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype

doi: 10.1016/j.jbo.2026.100754

Figure Lengend Snippet: Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Article Snippet: PC3 prostate tumour cells (ATCC CRL-1435), 4T1 breast tumour cells (CRL-2539) and K562 leukemia tumour cells (CCL-243) were obtained from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Co-Culture Assay, Control, Isolation, Cell Characterization

Cell–cell and cell–matrix interaction of PC3 par versus PC3 res cells. ( A ) Adhesion to HUVEC. PC3 par and PC3 res cells were treated with fresh medium (without RAD001) for 3 days and then added to HUVEC monolayers for 30, 60 or 120 min. ( B ) Adhesion to extracellular matrix proteins. PC3 par and PC3 res cells were treated with fresh medium (without RAD001) for 3 days and then added to immobilised collagen, laminin or fibronectin for 60 min. The adhesion rate of PC3 par versus PC3 res cells was compared in both experimental settings. Adhesion rate of PC3 par and PC3 res cells was also compared with the number of PC3 par and PC3 res cells treated with fresh medium for 3 days and subsequently with 5 nℳ RAD001. Mean values were calculated from five counts. Mean adhesion ( A ) or binding capacity ( B ) is depicted as adherent cells per 0.25 mm 2 . One representative of six experiments is shown. *indicates significant difference between the PC3 subline not treated with 5 nℳ RAD001 and the PC3 subline treated with 5 nℳ RAD001. # indicates significant difference between PC3 par and PC3 res cells.

Journal: British Journal of Cancer

Article Title: Resistance to the mTOR-inhibitor RAD001 elevates integrin α 2- and β 1-triggered motility, migration and invasion of prostate cancer cells

doi: 10.1038/bjc.2012.313

Figure Lengend Snippet: Cell–cell and cell–matrix interaction of PC3 par versus PC3 res cells. ( A ) Adhesion to HUVEC. PC3 par and PC3 res cells were treated with fresh medium (without RAD001) for 3 days and then added to HUVEC monolayers for 30, 60 or 120 min. ( B ) Adhesion to extracellular matrix proteins. PC3 par and PC3 res cells were treated with fresh medium (without RAD001) for 3 days and then added to immobilised collagen, laminin or fibronectin for 60 min. The adhesion rate of PC3 par versus PC3 res cells was compared in both experimental settings. Adhesion rate of PC3 par and PC3 res cells was also compared with the number of PC3 par and PC3 res cells treated with fresh medium for 3 days and subsequently with 5 nℳ RAD001. Mean values were calculated from five counts. Mean adhesion ( A ) or binding capacity ( B ) is depicted as adherent cells per 0.25 mm 2 . One representative of six experiments is shown. *indicates significant difference between the PC3 subline not treated with 5 nℳ RAD001 and the PC3 subline treated with 5 nℳ RAD001. # indicates significant difference between PC3 par and PC3 res cells.

Article Snippet: The human prostate tumour cell line PC3 was obtained from DSMZ (Braunschweig, Germany).

Techniques: Binding Assay

RAD001 resistance alters PC3 chemotaxis ( A, D ), migration ( B ) and invasion ( C ) as assessed in a Transwell chamber assay. PC3 par and PC3 res cells were used, as well as PC3 par and PC3 res cells, additionally treated with 5 nℳ RAD001, as indicated in Materials and Methods. To evaluate chemotaxis, tumour cells were seeded in the upper chamber in serum-free medium, and 10% FCS, as the chemoattractant, was placed in the lower well. To evaluate cell migration, Transwell chambers were precoated with collagen. Invasion was analysed by adding the tumour cells to the upper chamber, which was coated with collagen and overlaid with HUVEC. Cells, which moved to the lower surface of the membrane, were stained using hematoxylin and counted. ( D ) Representative chemotaxis assays. Mean values were calculated from five counts and depicted as cell number per 0.25 mm 2 . One representative of six experiments is shown. *indicates significant difference between the PC3 subline not treated with 5 nℳ RAD001 and the PC3 subline treated with 5 nℳ RAD001. # indicates significant difference between PC3 par and PC3 res cells.

Journal: British Journal of Cancer

Article Title: Resistance to the mTOR-inhibitor RAD001 elevates integrin α 2- and β 1-triggered motility, migration and invasion of prostate cancer cells

doi: 10.1038/bjc.2012.313

Figure Lengend Snippet: RAD001 resistance alters PC3 chemotaxis ( A, D ), migration ( B ) and invasion ( C ) as assessed in a Transwell chamber assay. PC3 par and PC3 res cells were used, as well as PC3 par and PC3 res cells, additionally treated with 5 nℳ RAD001, as indicated in Materials and Methods. To evaluate chemotaxis, tumour cells were seeded in the upper chamber in serum-free medium, and 10% FCS, as the chemoattractant, was placed in the lower well. To evaluate cell migration, Transwell chambers were precoated with collagen. Invasion was analysed by adding the tumour cells to the upper chamber, which was coated with collagen and overlaid with HUVEC. Cells, which moved to the lower surface of the membrane, were stained using hematoxylin and counted. ( D ) Representative chemotaxis assays. Mean values were calculated from five counts and depicted as cell number per 0.25 mm 2 . One representative of six experiments is shown. *indicates significant difference between the PC3 subline not treated with 5 nℳ RAD001 and the PC3 subline treated with 5 nℳ RAD001. # indicates significant difference between PC3 par and PC3 res cells.

Article Snippet: The human prostate tumour cell line PC3 was obtained from DSMZ (Braunschweig, Germany).

Techniques: Chemotaxis Assay, Migration, Transwell Chamber Assay, Membrane, Staining

FACS analysis of integrin α and β subtype expression on PC3 par versus PC3 res cells. Cells were washed in blocking solution and then stained with specific monoclonal antibodies as listed in Materials and Methods. To evaluate background staining of PE-conjugated antibodies, goat anti-mouse IgG1-PE or IgG2a-PE was used (dotted lines). Fluorescence was analysed using a FACScan flow cytometer. Mean fluorescence values are given below the histograms. One from three independent experiments.

Journal: British Journal of Cancer

Article Title: Resistance to the mTOR-inhibitor RAD001 elevates integrin α 2- and β 1-triggered motility, migration and invasion of prostate cancer cells

doi: 10.1038/bjc.2012.313

Figure Lengend Snippet: FACS analysis of integrin α and β subtype expression on PC3 par versus PC3 res cells. Cells were washed in blocking solution and then stained with specific monoclonal antibodies as listed in Materials and Methods. To evaluate background staining of PE-conjugated antibodies, goat anti-mouse IgG1-PE or IgG2a-PE was used (dotted lines). Fluorescence was analysed using a FACScan flow cytometer. Mean fluorescence values are given below the histograms. One from three independent experiments.

Article Snippet: The human prostate tumour cell line PC3 was obtained from DSMZ (Braunschweig, Germany).

Techniques: Expressing, Blocking Assay, Staining, Bioprocessing, Fluorescence, Flow Cytometry

Modification of intracellular integrin protein level. ( A ) Lysates of PC3 par or PC3 res cells were subjected to SDS–PAGE and blotted on the membrane incubated with respective monoclonal antibodies. β -actin served as the internal control. The figure shows one representative from three separate experiments. ( B ) is related to the integrin gene-expression pattern. Primer sets used for evaluation are listed in materials and methods. Calculation of the relative expression of each gene was done by the ΔΔCt method in the analysis programme of SABioscience Corporation. The housekeeping gene GAPDH was used for normalisation. Values are given as fold difference to PC3 par cells. *indicates significant difference.

Journal: British Journal of Cancer

Article Title: Resistance to the mTOR-inhibitor RAD001 elevates integrin α 2- and β 1-triggered motility, migration and invasion of prostate cancer cells

doi: 10.1038/bjc.2012.313

Figure Lengend Snippet: Modification of intracellular integrin protein level. ( A ) Lysates of PC3 par or PC3 res cells were subjected to SDS–PAGE and blotted on the membrane incubated with respective monoclonal antibodies. β -actin served as the internal control. The figure shows one representative from three separate experiments. ( B ) is related to the integrin gene-expression pattern. Primer sets used for evaluation are listed in materials and methods. Calculation of the relative expression of each gene was done by the ΔΔCt method in the analysis programme of SABioscience Corporation. The housekeeping gene GAPDH was used for normalisation. Values are given as fold difference to PC3 par cells. *indicates significant difference.

Article Snippet: The human prostate tumour cell line PC3 was obtained from DSMZ (Braunschweig, Germany).

Techniques: Modification, SDS Page, Membrane, Incubation, Bioprocessing, Control, Gene Expression, Expressing

Western blot analysis of cell signalling proteins, listed in methods. PC3 par or PC3 res cells remained untreated (control). They were kept for 2 h in serum-free cell culture medium and subsequently stimulated for 30 min with EGF (100 ng ml −1 ; +EGF) or they were stimulated with EGF and additionally treated with 5 nℳ RAD001 (+EGF+RAD001). Cell lysates were then subjected to SDS–PAGE and blotted on the membrane incubated with the respective monoclonal antibodies. β -actin served as the internal control. The figure shows one representative from three separate experiments.

Journal: British Journal of Cancer

Article Title: Resistance to the mTOR-inhibitor RAD001 elevates integrin α 2- and β 1-triggered motility, migration and invasion of prostate cancer cells

doi: 10.1038/bjc.2012.313

Figure Lengend Snippet: Western blot analysis of cell signalling proteins, listed in methods. PC3 par or PC3 res cells remained untreated (control). They were kept for 2 h in serum-free cell culture medium and subsequently stimulated for 30 min with EGF (100 ng ml −1 ; +EGF) or they were stimulated with EGF and additionally treated with 5 nℳ RAD001 (+EGF+RAD001). Cell lysates were then subjected to SDS–PAGE and blotted on the membrane incubated with the respective monoclonal antibodies. β -actin served as the internal control. The figure shows one representative from three separate experiments.

Article Snippet: The human prostate tumour cell line PC3 was obtained from DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Control, Cell Culture, SDS Page, Membrane, Incubation, Bioprocessing

Influence of integrin α 2, α 5 or β 1 blockade on tumour cell adhesion, chemotaxis or migration. PC3 par or PC3 res cells were preincubated for 60 min with function-blocking anti-integrin β 1, anti-integrin α 2 or anti-integrin α 5 monoclonal antibodies. Controls remained untreated. Cells were then subjected to the adhesion, chemotaxis and migration assay as indicated in Materials and Methods. Values are shown as percentage difference to the 100% control. *indicates significant difference between the PC3 control subline and the PC3 subline treated with the function-blocking antibody. # indicates significant difference between PC3 par and PC3 res cells whose integrin subtype was blocked.

Journal: British Journal of Cancer

Article Title: Resistance to the mTOR-inhibitor RAD001 elevates integrin α 2- and β 1-triggered motility, migration and invasion of prostate cancer cells

doi: 10.1038/bjc.2012.313

Figure Lengend Snippet: Influence of integrin α 2, α 5 or β 1 blockade on tumour cell adhesion, chemotaxis or migration. PC3 par or PC3 res cells were preincubated for 60 min with function-blocking anti-integrin β 1, anti-integrin α 2 or anti-integrin α 5 monoclonal antibodies. Controls remained untreated. Cells were then subjected to the adhesion, chemotaxis and migration assay as indicated in Materials and Methods. Values are shown as percentage difference to the 100% control. *indicates significant difference between the PC3 control subline and the PC3 subline treated with the function-blocking antibody. # indicates significant difference between PC3 par and PC3 res cells whose integrin subtype was blocked.

Article Snippet: The human prostate tumour cell line PC3 was obtained from DSMZ (Braunschweig, Germany).

Techniques: Chemotaxis Assay, Migration, Blocking Assay, Bioprocessing, Control

Effects of ACS2 (2A) or ACS33 (2B) on prostate cancer proliferation in vitro. DU-145 or PC3 cells were treated with various concentrations of ACS2 or ACS33 for 3 or 5 days, or remained un-treated (control). Cell proliferation was then assessed using the MTT dye reduction assay. Cell numbers at day 2 (48 hrs) were normalized to the number of day 1 (24 hrs, as 100%). One representative of six experiments is shown. * indicates significant difference to controls.

Journal: Journal of Cellular and Molecular Medicine

Article Title: New histone deacetylase inhibitors as potential therapeutic tools for advanced prostate carcinoma

doi: 10.1111/j.1582-4934.2008.00271.x

Figure Lengend Snippet: Effects of ACS2 (2A) or ACS33 (2B) on prostate cancer proliferation in vitro. DU-145 or PC3 cells were treated with various concentrations of ACS2 or ACS33 for 3 or 5 days, or remained un-treated (control). Cell proliferation was then assessed using the MTT dye reduction assay. Cell numbers at day 2 (48 hrs) were normalized to the number of day 1 (24 hrs, as 100%). One representative of six experiments is shown. * indicates significant difference to controls.

Article Snippet: Human prostate tumour cell lines PC3 and DU-145 were obtained from DSMZ (Braunschweig, Germany).

Techniques: In Vitro, Control, MTT Reduction Assay

Adhesion of prostate cancer cells to human endothelial cells (HUVEC) is down-regulated by ACS2 (3A) or ACS33 (3B). DU-145 or PC3 cells were treated with various concentrations of ACS2 or ACS33 for 3 or 5 days, and then added at a density of 0.5 × 10 6 cells/well to HUVEC monolayers for different time periods. Non-adherent tumour cells were washed off in each sample; the remaining cells were fixed and counted in five different fields (5 × 0.25 mm 2 ) using a phase contrast microscope. Mean values were calculated from five counts. Mean adhesion capacity is depicted as counted cells/mm 2 . One representative of six experiments is shown. * Indicates significant difference to controls.

Journal: Journal of Cellular and Molecular Medicine

Article Title: New histone deacetylase inhibitors as potential therapeutic tools for advanced prostate carcinoma

doi: 10.1111/j.1582-4934.2008.00271.x

Figure Lengend Snippet: Adhesion of prostate cancer cells to human endothelial cells (HUVEC) is down-regulated by ACS2 (3A) or ACS33 (3B). DU-145 or PC3 cells were treated with various concentrations of ACS2 or ACS33 for 3 or 5 days, and then added at a density of 0.5 × 10 6 cells/well to HUVEC monolayers for different time periods. Non-adherent tumour cells were washed off in each sample; the remaining cells were fixed and counted in five different fields (5 × 0.25 mm 2 ) using a phase contrast microscope. Mean values were calculated from five counts. Mean adhesion capacity is depicted as counted cells/mm 2 . One representative of six experiments is shown. * Indicates significant difference to controls.

Article Snippet: Human prostate tumour cell lines PC3 and DU-145 were obtained from DSMZ (Braunschweig, Germany).

Techniques: Microscopy

ACS33 prevents destruction of the endothelial cell monolayer induced by prostate tumour cells. Morphological analysis is shown. 4 hrs after adding DU-145 or PC3 tumour cells to HUVEC, round openings appear in the endothelial monolayer in the course of tumour cell binding (arrows). Application of ACS33 prevents focal disruptions of intercellular endothelial connections (right hand; both: phase contrast, × 20 objective).

Journal: Journal of Cellular and Molecular Medicine

Article Title: New histone deacetylase inhibitors as potential therapeutic tools for advanced prostate carcinoma

doi: 10.1111/j.1582-4934.2008.00271.x

Figure Lengend Snippet: ACS33 prevents destruction of the endothelial cell monolayer induced by prostate tumour cells. Morphological analysis is shown. 4 hrs after adding DU-145 or PC3 tumour cells to HUVEC, round openings appear in the endothelial monolayer in the course of tumour cell binding (arrows). Application of ACS33 prevents focal disruptions of intercellular endothelial connections (right hand; both: phase contrast, × 20 objective).

Article Snippet: Human prostate tumour cell lines PC3 and DU-145 were obtained from DSMZ (Braunschweig, Germany).

Techniques: Binding Assay

Western blot analysis of H3 and H4 histone expression (total and acetylated) in ACS-treated- and non-treated cells. DU-145 or PC3 cells were incubated with ACS2 or ACS33 for 24 hrs. Cell lysates were then analysed by specific antibodies as listed in materials and methods. β-actin served as the internal control. One representative experiment of three is shown.

Journal: Journal of Cellular and Molecular Medicine

Article Title: New histone deacetylase inhibitors as potential therapeutic tools for advanced prostate carcinoma

doi: 10.1111/j.1582-4934.2008.00271.x

Figure Lengend Snippet: Western blot analysis of H3 and H4 histone expression (total and acetylated) in ACS-treated- and non-treated cells. DU-145 or PC3 cells were incubated with ACS2 or ACS33 for 24 hrs. Cell lysates were then analysed by specific antibodies as listed in materials and methods. β-actin served as the internal control. One representative experiment of three is shown.

Article Snippet: Human prostate tumour cell lines PC3 and DU-145 were obtained from DSMZ (Braunschweig, Germany).

Techniques: Western Blot, Expressing, Incubation, Control

Effect of ACS33 on prostate cancer xenografts. PC3 xenografts were established in male athymic mice. Animals in the treatment arm received 20 mg/kg bw ACS33 each day, or 2 mg cisplatin/kg/day (cis-pt). *Indicates significant difference to the control animals. Western blot analysis of H3 and H4 histone expression (total and acetylated), of bcl-2, bax, ILK and Fak (total and activated) was carried out on the tissue specimens using specific antibodies as listed in materials and methods (Fig. , right). β-actin served as the internal control. One representative western blot data of three are shown.

Journal: Journal of Cellular and Molecular Medicine

Article Title: New histone deacetylase inhibitors as potential therapeutic tools for advanced prostate carcinoma

doi: 10.1111/j.1582-4934.2008.00271.x

Figure Lengend Snippet: Effect of ACS33 on prostate cancer xenografts. PC3 xenografts were established in male athymic mice. Animals in the treatment arm received 20 mg/kg bw ACS33 each day, or 2 mg cisplatin/kg/day (cis-pt). *Indicates significant difference to the control animals. Western blot analysis of H3 and H4 histone expression (total and acetylated), of bcl-2, bax, ILK and Fak (total and activated) was carried out on the tissue specimens using specific antibodies as listed in materials and methods (Fig. , right). β-actin served as the internal control. One representative western blot data of three are shown.

Article Snippet: Human prostate tumour cell lines PC3 and DU-145 were obtained from DSMZ (Braunschweig, Germany).

Techniques: Control, Western Blot, Expressing

Histological examination of the PC3 tumour xenografts growing s.c. in male athymic mice. Representative pictures are shown. Immunostaining of MIB (dark red reaction product) documents a decreased tumour cell proliferation. Enhanced immunostaining of acetylated H3 indicates HDAC-inhibitory activity of ACS33.

Journal: Journal of Cellular and Molecular Medicine

Article Title: New histone deacetylase inhibitors as potential therapeutic tools for advanced prostate carcinoma

doi: 10.1111/j.1582-4934.2008.00271.x

Figure Lengend Snippet: Histological examination of the PC3 tumour xenografts growing s.c. in male athymic mice. Representative pictures are shown. Immunostaining of MIB (dark red reaction product) documents a decreased tumour cell proliferation. Enhanced immunostaining of acetylated H3 indicates HDAC-inhibitory activity of ACS33.

Article Snippet: Human prostate tumour cell lines PC3 and DU-145 were obtained from DSMZ (Braunschweig, Germany).

Techniques: Immunostaining, Activity Assay

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1) Product Images from "Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype"

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