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ATCC human prostate cancer pca cell lines du145
Human Prostate Cancer Pca Cell Lines Du145, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human prostate cancer pca cell lines du145 - by Bioz Stars, 2026-03
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ATCC du145 human prostate cancer cell line
GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in <t>DU145</t> cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Du145 Human Prostate Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/du145 human prostate cancer cell line/product/ATCC
Average 99 stars, based on 1 article reviews
du145 human prostate cancer cell line - by Bioz Stars, 2026-03
99/100 stars
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99
ATCC human prostate cancer cell line du145
GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in <t>DU145</t> cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Human Prostate Cancer Cell Line Du145, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human prostate cancer cell line du145/product/ATCC
Average 99 stars, based on 1 article reviews
human prostate cancer cell line du145 - by Bioz Stars, 2026-03
99/100 stars
  Buy from Supplier

99
ATCC tissue culture prostate cancer cell lines du145
GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in <t>DU145</t> cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Tissue Culture Prostate Cancer Cell Lines Du145, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/tissue culture prostate cancer cell lines du145/product/ATCC
Average 99 stars, based on 1 article reviews
tissue culture prostate cancer cell lines du145 - by Bioz Stars, 2026-03
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99
ATCC du145 prostatic human cancer cell lines
Effects of the different fruit extracts on the proliferation of the colon cancer cell line HCT116 and the prostate cancer cell line <t>DU145</t> . DU145 (A) or HCT116 (B) were seeded in a 12-well plate and allowed to grow for 12 h. Then, 500 μg/mLof PBS-resuspended extract derived from the pulp, seeds, and skin of Meliccocus oliviformis , Nephelium lappaceum , and Manilkara zapota were added and cell proliferation was monitored by analyzing the surface area occupied by the cells in each well (% confluence) from photos taken at regular intervals (every 3 h) by the Incucyte live cell imaging system over a period of three days. Data shown are the average ± SD of three independent experiments.
Du145 Prostatic Human Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/du145 prostatic human cancer cell lines/product/ATCC
Average 99 stars, based on 1 article reviews
du145 prostatic human cancer cell lines - by Bioz Stars, 2026-03
99/100 stars
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99
ATCC prostate cancer cell lines du145
Erastin induced ferroptosis of prostate cancer cells. A Viability of <t>DU145,</t> LNCaP and PC3 cells exposed to various concentrations of Erastin for 72 h. n = 3, *** p < 0.001. B Dose effect of Erastin on cellular lipid ROS accumulation by using DCF-DA probe in DU145 cells incubated with Erastin for 24 h. n = 3, ** p < 0.01, versus to control. C Time course effect of Erastin on cellular lipid ROS accumulation by using DCF-DA probe in DU145 cells incubated with 1 µM Erastin. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001 versus to control. D and E Colony formation assay of DU145 exposed to Erastin, RSL3, liproxstain-1 or combo as indicated for 72 h. ** p < 0.01, *** p < 0.001versus to control; ## p < 0.01, ### p < 0.001versus to Erastin or RSL3 alone. F Visualization of DU145 cells viability under exposure to Erastin (8 µM), deferoxamine (DFO, 12.5 µM) and combo for 72 h. The magnification is 100×
Prostate Cancer Cell Lines Du145, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/prostate cancer cell lines du145/product/ATCC
Average 99 stars, based on 1 article reviews
prostate cancer cell lines du145 - by Bioz Stars, 2026-03
99/100 stars
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99
ATCC du145 prostate cancer cell lines
ACTC1 promotes prostate cancer cell proliferation and migration. A . Cell proliferation was measured at the indicated time points in LNCaP, PC-3 and <t>DU145</t> cells (** P < 0.01, *** P < 0.001, N = 3). Error bar: mean ± SEM. B . promotes prostate cancer cell proliferation. Transwell assay analyses of the indicated cell lines ( N = 3). Error bar: mean ± SEM. C . Xenograft analyses of DU145-derived tumors with control vector or ACTC1 overexpression (** P < 0.01, *** P < 0.001). Error bar: mean ± SEM
Du145 Prostate Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/du145 prostate cancer cell lines/product/ATCC
Average 99 stars, based on 1 article reviews
du145 prostate cancer cell lines - by Bioz Stars, 2026-03
99/100 stars
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GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in DU145 cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: Frontiers in Immunology

Article Title: Identify GDPD3 as a key regulator of epithelial–mesenchymal transition and prostate adenocarcinoma progression via the LPA/LPAR1/AKT axis: transcriptomic and experimental study

doi: 10.3389/fimmu.2025.1637325

Figure Lengend Snippet: GDPD3 promotes EMT through LPA–LPAR1 signaling. (A) Analysis of the correlation between GDPD3 and LPA. (B) LPA levels were measured by ELISA following GDPD3 overexpression in DU145 cells. (C) DU145 cells were treated with either vehicle control or 20 μM LPA for 24, 48, and 72 hours. Protein levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. (D, E) DU145 cells were treated with LPA alone, or with LPA in combination with KI6425 or AM095 (both LPAR1 inhibitors). EMT markers N-cadherin, Vimentin and α-SMA were evaluated by Western blot, and band intensities were quantified using ImageJ software, normalized to actin. (n = 3–4 independent experiments). Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: The DU145 human prostate cancer cell line was obtained from the American Type Culture Collection (ATCC) in February 2025.

Techniques: Enzyme-linked Immunosorbent Assay, Over Expression, Control, Western Blot, Software

LPAR1 knockdown and AKT inhibition attenuate LPA-induced EMT. (A, B) LPAR1 was knocked down, and knockdown efficiency was subsequently validated. (C, D) DU145 cells were transfected with siRNA targeting LPAR1, and the expression levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot. (E, F) Western blot analysis was performed to assess the expression levels of AKT and phosphorylated AKT (p-AKT). (G, H) DU145 cells were treated with 2 μM LY294002 (AKT pathway inhibitor), and the protein levels of AKT, phosphorylated AKT (p-AKT), N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. Band intensities were quantified using ImageJ software and normalized to actin. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: Frontiers in Immunology

Article Title: Identify GDPD3 as a key regulator of epithelial–mesenchymal transition and prostate adenocarcinoma progression via the LPA/LPAR1/AKT axis: transcriptomic and experimental study

doi: 10.3389/fimmu.2025.1637325

Figure Lengend Snippet: LPAR1 knockdown and AKT inhibition attenuate LPA-induced EMT. (A, B) LPAR1 was knocked down, and knockdown efficiency was subsequently validated. (C, D) DU145 cells were transfected with siRNA targeting LPAR1, and the expression levels of N-cadherin, E-cadherin and Vimentin were assessed by Western blot. (E, F) Western blot analysis was performed to assess the expression levels of AKT and phosphorylated AKT (p-AKT). (G, H) DU145 cells were treated with 2 μM LY294002 (AKT pathway inhibitor), and the protein levels of AKT, phosphorylated AKT (p-AKT), N-cadherin, E-cadherin and Vimentin were assessed by Western blot and quantified. Band intensities were quantified using ImageJ software and normalized to actin. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: The DU145 human prostate cancer cell line was obtained from the American Type Culture Collection (ATCC) in February 2025.

Techniques: Knockdown, Inhibition, Transfection, Expressing, Western Blot, Software

Effects of the different fruit extracts on the proliferation of the colon cancer cell line HCT116 and the prostate cancer cell line DU145 . DU145 (A) or HCT116 (B) were seeded in a 12-well plate and allowed to grow for 12 h. Then, 500 μg/mLof PBS-resuspended extract derived from the pulp, seeds, and skin of Meliccocus oliviformis , Nephelium lappaceum , and Manilkara zapota were added and cell proliferation was monitored by analyzing the surface area occupied by the cells in each well (% confluence) from photos taken at regular intervals (every 3 h) by the Incucyte live cell imaging system over a period of three days. Data shown are the average ± SD of three independent experiments.

Journal: Biochemistry and Biophysics Reports

Article Title: Investigating the ABTS-based antioxidant potential and antiproliferative activity of pulp, skin and seeds extracts from Nephelium lappaceum , Manilkara zapota , and Meliccocus oliviformis on human prostate and colon cancer cells

doi: 10.1016/j.bbrep.2025.102257

Figure Lengend Snippet: Effects of the different fruit extracts on the proliferation of the colon cancer cell line HCT116 and the prostate cancer cell line DU145 . DU145 (A) or HCT116 (B) were seeded in a 12-well plate and allowed to grow for 12 h. Then, 500 μg/mLof PBS-resuspended extract derived from the pulp, seeds, and skin of Meliccocus oliviformis , Nephelium lappaceum , and Manilkara zapota were added and cell proliferation was monitored by analyzing the surface area occupied by the cells in each well (% confluence) from photos taken at regular intervals (every 3 h) by the Incucyte live cell imaging system over a period of three days. Data shown are the average ± SD of three independent experiments.

Article Snippet: The HCT116 (colic), and DU145 (prostatic) human cancer cell lines were purchased from ATCC (American Type Culture Collection).

Techniques: Derivative Assay, Live Cell Imaging

Effects of the different fruit extracts on the viability of the colon cancer cell line HCT116 and the prostate cancer cell line DU145 . DU145 (A) or HCT116 (B) were seeded in a 12-well plate and allowed to grow for 12 h. Then, 500 μg/mL of PBS-resuspended extract derived from the pulp, seeds, and skin of Meliccocus oliviformis , Nephelium lappaceum , and Manilkara zapota were added. 24h later, cell viability was assessed using the MTT assay. Data shown are the average ± SD of three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, one-way ANOVA followed by Tukey's multiple comparison test.

Journal: Biochemistry and Biophysics Reports

Article Title: Investigating the ABTS-based antioxidant potential and antiproliferative activity of pulp, skin and seeds extracts from Nephelium lappaceum , Manilkara zapota , and Meliccocus oliviformis on human prostate and colon cancer cells

doi: 10.1016/j.bbrep.2025.102257

Figure Lengend Snippet: Effects of the different fruit extracts on the viability of the colon cancer cell line HCT116 and the prostate cancer cell line DU145 . DU145 (A) or HCT116 (B) were seeded in a 12-well plate and allowed to grow for 12 h. Then, 500 μg/mL of PBS-resuspended extract derived from the pulp, seeds, and skin of Meliccocus oliviformis , Nephelium lappaceum , and Manilkara zapota were added. 24h later, cell viability was assessed using the MTT assay. Data shown are the average ± SD of three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, one-way ANOVA followed by Tukey's multiple comparison test.

Article Snippet: The HCT116 (colic), and DU145 (prostatic) human cancer cell lines were purchased from ATCC (American Type Culture Collection).

Techniques: Derivative Assay, MTT Assay, Comparison

Erastin induced ferroptosis of prostate cancer cells. A Viability of DU145, LNCaP and PC3 cells exposed to various concentrations of Erastin for 72 h. n = 3, *** p < 0.001. B Dose effect of Erastin on cellular lipid ROS accumulation by using DCF-DA probe in DU145 cells incubated with Erastin for 24 h. n = 3, ** p < 0.01, versus to control. C Time course effect of Erastin on cellular lipid ROS accumulation by using DCF-DA probe in DU145 cells incubated with 1 µM Erastin. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001 versus to control. D and E Colony formation assay of DU145 exposed to Erastin, RSL3, liproxstain-1 or combo as indicated for 72 h. ** p < 0.01, *** p < 0.001versus to control; ## p < 0.01, ### p < 0.001versus to Erastin or RSL3 alone. F Visualization of DU145 cells viability under exposure to Erastin (8 µM), deferoxamine (DFO, 12.5 µM) and combo for 72 h. The magnification is 100×

Journal: Discover Oncology

Article Title: Ferroptotic resistance involved in PTEN-loss prostate cancer progression

doi: 10.1007/s12672-025-03990-2

Figure Lengend Snippet: Erastin induced ferroptosis of prostate cancer cells. A Viability of DU145, LNCaP and PC3 cells exposed to various concentrations of Erastin for 72 h. n = 3, *** p < 0.001. B Dose effect of Erastin on cellular lipid ROS accumulation by using DCF-DA probe in DU145 cells incubated with Erastin for 24 h. n = 3, ** p < 0.01, versus to control. C Time course effect of Erastin on cellular lipid ROS accumulation by using DCF-DA probe in DU145 cells incubated with 1 µM Erastin. n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001 versus to control. D and E Colony formation assay of DU145 exposed to Erastin, RSL3, liproxstain-1 or combo as indicated for 72 h. ** p < 0.01, *** p < 0.001versus to control; ## p < 0.01, ### p < 0.001versus to Erastin or RSL3 alone. F Visualization of DU145 cells viability under exposure to Erastin (8 µM), deferoxamine (DFO, 12.5 µM) and combo for 72 h. The magnification is 100×

Article Snippet: Prostate cancer cell lines DU145, PC3 and LNCaP were obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Incubation, Control, Colony Assay

PTEN loss led to ferroptotic resistance in prostate cancer cells. A and B Western blot analysis of PTEN expression in DU145, PC3, LNCaP and DU145 PTEN knockdown cells. C and D Viability of DU145 PTEN deficient cells exposed to various concentrations of Erastin or RSL3 for 72 h. n = 3, ** p < 0.01*** p < 0.001. E and F The left, colony formation assay of DU145 exposed to Erastin or RSL3 in DU145 PTEN deficient cells for 72 h; the right, quantity of colony was presented as mean ± SD. ** p < 0.01

Journal: Discover Oncology

Article Title: Ferroptotic resistance involved in PTEN-loss prostate cancer progression

doi: 10.1007/s12672-025-03990-2

Figure Lengend Snippet: PTEN loss led to ferroptotic resistance in prostate cancer cells. A and B Western blot analysis of PTEN expression in DU145, PC3, LNCaP and DU145 PTEN knockdown cells. C and D Viability of DU145 PTEN deficient cells exposed to various concentrations of Erastin or RSL3 for 72 h. n = 3, ** p < 0.01*** p < 0.001. E and F The left, colony formation assay of DU145 exposed to Erastin or RSL3 in DU145 PTEN deficient cells for 72 h; the right, quantity of colony was presented as mean ± SD. ** p < 0.01

Article Snippet: Prostate cancer cell lines DU145, PC3 and LNCaP were obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Western Blot, Expressing, Knockdown, Colony Assay

PTEN loss promoted transcription of GPX4. A and B Western blots analysis of AKT, p-AKT, NRF2 and GPX4 expression in DU145, PC3, LNCaP and DU145 PTEN deficient cells. C Cell viability was determined in DU145 with PTEN deficient cells under exposure to series concentration of Erastin combined with GDC0941 (0.25 µM) for 72 h. D and E mRNA expression of GPX4 and NRF2 was determined in DU145-PTEN-KD cells by qRT-PCR, *** p < 0.001. F Measurement of ROS level in DU145-PTEN-KD cells using DCF-DA probe. *** p < 0.001

Journal: Discover Oncology

Article Title: Ferroptotic resistance involved in PTEN-loss prostate cancer progression

doi: 10.1007/s12672-025-03990-2

Figure Lengend Snippet: PTEN loss promoted transcription of GPX4. A and B Western blots analysis of AKT, p-AKT, NRF2 and GPX4 expression in DU145, PC3, LNCaP and DU145 PTEN deficient cells. C Cell viability was determined in DU145 with PTEN deficient cells under exposure to series concentration of Erastin combined with GDC0941 (0.25 µM) for 72 h. D and E mRNA expression of GPX4 and NRF2 was determined in DU145-PTEN-KD cells by qRT-PCR, *** p < 0.001. F Measurement of ROS level in DU145-PTEN-KD cells using DCF-DA probe. *** p < 0.001

Article Snippet: Prostate cancer cell lines DU145, PC3 and LNCaP were obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Western Blot, Expressing, Concentration Assay, Quantitative RT-PCR

Knockdown of GPX4 restored sensitivity of cells to ferroptosis inducer. A Efficacy of shRNA targeting GPX4 was determined in PTEN deficient DU145 cells by western blot. B and C Sensitivity of DU145 cells with PTEN and GPX4 double deficient to Erastin or RSL3 was determined by MTT assay, n = 3, ** p < 0.01, *** p < 0.001 vs. control. D Efficacy of shRNA targeting GPX4 was determined in LNCaP cells by western blot. E Sensitivity of LNCaP cells with GPX4 deficient to Erastin was determined by MTT assay. n = 3, ** p < 0.01, *** p < 0.001 vs. control

Journal: Discover Oncology

Article Title: Ferroptotic resistance involved in PTEN-loss prostate cancer progression

doi: 10.1007/s12672-025-03990-2

Figure Lengend Snippet: Knockdown of GPX4 restored sensitivity of cells to ferroptosis inducer. A Efficacy of shRNA targeting GPX4 was determined in PTEN deficient DU145 cells by western blot. B and C Sensitivity of DU145 cells with PTEN and GPX4 double deficient to Erastin or RSL3 was determined by MTT assay, n = 3, ** p < 0.01, *** p < 0.001 vs. control. D Efficacy of shRNA targeting GPX4 was determined in LNCaP cells by western blot. E Sensitivity of LNCaP cells with GPX4 deficient to Erastin was determined by MTT assay. n = 3, ** p < 0.01, *** p < 0.001 vs. control

Article Snippet: Prostate cancer cell lines DU145, PC3 and LNCaP were obtained from American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Knockdown, shRNA, Western Blot, MTT Assay, Control

ACTC1 promotes prostate cancer cell proliferation and migration. A . Cell proliferation was measured at the indicated time points in LNCaP, PC-3 and DU145 cells (** P < 0.01, *** P < 0.001, N = 3). Error bar: mean ± SEM. B . promotes prostate cancer cell proliferation. Transwell assay analyses of the indicated cell lines ( N = 3). Error bar: mean ± SEM. C . Xenograft analyses of DU145-derived tumors with control vector or ACTC1 overexpression (** P < 0.01, *** P < 0.001). Error bar: mean ± SEM

Journal: BMC Cancer

Article Title: ACTC1 promotes tumor progression by upregulating BMP4 expression in prostate cancer

doi: 10.1186/s12885-025-15336-w

Figure Lengend Snippet: ACTC1 promotes prostate cancer cell proliferation and migration. A . Cell proliferation was measured at the indicated time points in LNCaP, PC-3 and DU145 cells (** P < 0.01, *** P < 0.001, N = 3). Error bar: mean ± SEM. B . promotes prostate cancer cell proliferation. Transwell assay analyses of the indicated cell lines ( N = 3). Error bar: mean ± SEM. C . Xenograft analyses of DU145-derived tumors with control vector or ACTC1 overexpression (** P < 0.01, *** P < 0.001). Error bar: mean ± SEM

Article Snippet: LNCaP, PC-3, and DU145 prostate cancer cell lines were obtained from ATCC (Bethesda, USA).

Techniques: Migration, Transwell Assay, Derivative Assay, Control, Plasmid Preparation, Over Expression

ACTC1 promotes prostate cancer cell proliferation by upregulating BMP4 expression. A .Volcano plot for DEGs in ACTC1-overexpressing DU145 RNA-seq. B .The GO enrichment terms of DEGs. C .KEGG pathway analysis of DEGs. D .RT‒qPCR analyses of the mRNA levels of BMP4 gene in prostate cancer cells with a control vector or ACTC1 overexpression (* P < 0.05, *** P < 0.001, N = 3). Error bar: mean ± SEM. E . BMP4 overexpression rescued the ACTC1-KD-mediated decrease in cell proliferation in DU145 cells. One-way ANOVA was used (** P < 0.01, *** P < 0.001, N = 3). Error bar: mean ± SEM F. BMP4 overexpression rescued ACTC1-KD-mediated defects in cell clone formation (*** P < 0.001, N = 3). Error bar: mean ± SEM

Journal: BMC Cancer

Article Title: ACTC1 promotes tumor progression by upregulating BMP4 expression in prostate cancer

doi: 10.1186/s12885-025-15336-w

Figure Lengend Snippet: ACTC1 promotes prostate cancer cell proliferation by upregulating BMP4 expression. A .Volcano plot for DEGs in ACTC1-overexpressing DU145 RNA-seq. B .The GO enrichment terms of DEGs. C .KEGG pathway analysis of DEGs. D .RT‒qPCR analyses of the mRNA levels of BMP4 gene in prostate cancer cells with a control vector or ACTC1 overexpression (* P < 0.05, *** P < 0.001, N = 3). Error bar: mean ± SEM. E . BMP4 overexpression rescued the ACTC1-KD-mediated decrease in cell proliferation in DU145 cells. One-way ANOVA was used (** P < 0.01, *** P < 0.001, N = 3). Error bar: mean ± SEM F. BMP4 overexpression rescued ACTC1-KD-mediated defects in cell clone formation (*** P < 0.001, N = 3). Error bar: mean ± SEM

Article Snippet: LNCaP, PC-3, and DU145 prostate cancer cell lines were obtained from ATCC (Bethesda, USA).

Techniques: Expressing, RNA Sequencing, Control, Plasmid Preparation, Over Expression