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ATCC human oc cell lines skov3

Effects of GEM on hypoxia‐inducible factor 1‐alpha (HIF1A), UBR5, and ovarian cancer Cells. (A) Western blot (WB) analysis of HIF1A and UBR5 expression in <t>SKOV3</t> cells under hypoxic conditions treated with different concentrations of GEM; (B) WB analysis of HIF1A and UBR5 expression in OVCAR‐3 cells under hypoxic conditions treated with different concentrations of GEM; (C) CCK‐8 assay of cell viability in SKOV3 cells treated with varying concentrations of GEM at 0, 24, and 48 h; (D) CCK‐8 assay of cell viability in OVCAR‐3 cells treated with varying concentrations of GEM at 0, 24, and 48 h; (E) wound healing assay assessing the migration rate of SKOV3 cells treated with different concentrations of GEM at 0 h, 24 h, and 48 h (scale bar: 100 μm); (F) wound healing assay assessing the migration rate of OVCAR‐3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 100 μm); (G) transwell invasion assay evaluating the invasive capacity of SKOV3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 50 μm); (H) transwell invasion assay evaluating the invasive capacity of OVCAR‐3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 50 μm). Data are presented as mean ± SD; all cellular experiments were performed in triplicate. *** p < 0.001, analyzed using ANOVA followed by Tukey's multiple comparison test.

Human Oc Cell Lines Skov3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7641 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human oc cell lines skov3 - by Bioz Stars, 2026-09

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1) Product Images from "Gemcitabine activates the Hippo signaling pathway and suppresses tumor growth by stabilizing large tumor suppressor kinase 2 through the hypoxia‐inducible factor 1‐alpha/ubiquitin protein ligase E3 component N‐recognin 5 axis"

Article Title: Gemcitabine activates the Hippo signaling pathway and suppresses tumor growth by stabilizing large tumor suppressor kinase 2 through the hypoxia‐inducible factor 1‐alpha/ubiquitin protein ligase E3 component N‐recognin 5 axis

Journal: Journal of Cell Communication and Signaling

doi: 10.1002/ccs3.70085

Figure Legend Snippet: Effects of GEM on hypoxia‐inducible factor 1‐alpha (HIF1A), UBR5, and ovarian cancer Cells. (A) Western blot (WB) analysis of HIF1A and UBR5 expression in SKOV3 cells under hypoxic conditions treated with different concentrations of GEM; (B) WB analysis of HIF1A and UBR5 expression in OVCAR‐3 cells under hypoxic conditions treated with different concentrations of GEM; (C) CCK‐8 assay of cell viability in SKOV3 cells treated with varying concentrations of GEM at 0, 24, and 48 h; (D) CCK‐8 assay of cell viability in OVCAR‐3 cells treated with varying concentrations of GEM at 0, 24, and 48 h; (E) wound healing assay assessing the migration rate of SKOV3 cells treated with different concentrations of GEM at 0 h, 24 h, and 48 h (scale bar: 100 μm); (F) wound healing assay assessing the migration rate of OVCAR‐3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 100 μm); (G) transwell invasion assay evaluating the invasive capacity of SKOV3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 50 μm); (H) transwell invasion assay evaluating the invasive capacity of OVCAR‐3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 50 μm). Data are presented as mean ± SD; all cellular experiments were performed in triplicate. *** p < 0.001, analyzed using ANOVA followed by Tukey's multiple comparison test.

Techniques Used: Western Blot, Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Comparison

Effects of GEM on ovarian cancer proliferation and invasion via HIF1A‐mediated downregulation of UBR5. (A) Western blot (WB) analysis of hypoxia‐inducible factor 1‐alpha (HIF1A) and UBR5 expression levels in SKOV3 cells treated with 20 μM GEM for 48 h; (B) WB analysis of HIF1A and UBR5 expression levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (C) CCK8 assay showing cell viability of SKOV3 cells treated with 20 μM GEM for 48 h; (D) CCK8 assay showing cell viability of OVCAR‐3 cells treated with 20 μM GEM for 48 h; (E) wound healing assay assessing the migration rate of SKOV3 cells treated with 20 μM GEM for 48 h (Scale bar: 100 μm); (F) wound healing assay assessing the migration rate of OVCAR‐3 cells treated with 20 μM GEM for 48 h (Scale bar: 100 μm); (G) transwell invasion assay showing the invasive capacity of SKOV3 cells treated with 20 μM GEM for 48 h (Scale bar: 50 μm); (H) transwell invasion assay showing the invasive capacity of OVCAR‐3 cells treated with 20 μM GEM for 48 h (Scale bar: 50 μm); (I) predicted transcription factor binding sites in the UBR5 promoter region based on JASPAR database analysis; (J) ChIP‐PCR analysis showing HIF1A enrichment at the UBR5 promoter region; (K) dual‐luciferase reporter assay evaluating the regulatory effect of HIF1A on UBR5 promoter activity; (L, M) RT‐qPCR analysis of HIF1A and UBR5 mRNA expression levels after shHIF1A knockdown in SKOV3 and OVCAR‐3 cells; (N, O) RT‐qPCR analysis of UBR5 mRNA expression levels in SKOV3 and OVCAR‐3 cells under normoxia, hypoxia, hypoxia + shNC, and hypoxia + shHIF1A conditions. Data are presented as mean ± SD; all cell experiments were performed in triplicate. *** p < 0.001, analyzed by ANOVA followed by Tukey's multiple comparison test.

Figure Legend Snippet: Effects of GEM on ovarian cancer proliferation and invasion via HIF1A‐mediated downregulation of UBR5. (A) Western blot (WB) analysis of hypoxia‐inducible factor 1‐alpha (HIF1A) and UBR5 expression levels in SKOV3 cells treated with 20 μM GEM for 48 h; (B) WB analysis of HIF1A and UBR5 expression levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (C) CCK8 assay showing cell viability of SKOV3 cells treated with 20 μM GEM for 48 h; (D) CCK8 assay showing cell viability of OVCAR‐3 cells treated with 20 μM GEM for 48 h; (E) wound healing assay assessing the migration rate of SKOV3 cells treated with 20 μM GEM for 48 h (Scale bar: 100 μm); (F) wound healing assay assessing the migration rate of OVCAR‐3 cells treated with 20 μM GEM for 48 h (Scale bar: 100 μm); (G) transwell invasion assay showing the invasive capacity of SKOV3 cells treated with 20 μM GEM for 48 h (Scale bar: 50 μm); (H) transwell invasion assay showing the invasive capacity of OVCAR‐3 cells treated with 20 μM GEM for 48 h (Scale bar: 50 μm); (I) predicted transcription factor binding sites in the UBR5 promoter region based on JASPAR database analysis; (J) ChIP‐PCR analysis showing HIF1A enrichment at the UBR5 promoter region; (K) dual‐luciferase reporter assay evaluating the regulatory effect of HIF1A on UBR5 promoter activity; (L, M) RT‐qPCR analysis of HIF1A and UBR5 mRNA expression levels after shHIF1A knockdown in SKOV3 and OVCAR‐3 cells; (N, O) RT‐qPCR analysis of UBR5 mRNA expression levels in SKOV3 and OVCAR‐3 cells under normoxia, hypoxia, hypoxia + shNC, and hypoxia + shHIF1A conditions. Data are presented as mean ± SD; all cell experiments were performed in triplicate. *** p < 0.001, analyzed by ANOVA followed by Tukey's multiple comparison test.

Techniques Used: Western Blot, Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Quantitative RT-PCR, Knockdown, Comparison

GEM regulates LATS2 ubiquitination and YAP/TAZ phosphorylation via the hypoxia‐inducible factor 1‐alpha/UBR5 axis. (A) Western blot (WB) analysis of Hippo pathway‐related proteins in SKOV3 cells under hypoxic conditions; (B) WB analysis of Hippo pathway‐related proteins in OVCAR‐3 cells under hypoxic conditions; (C) co‐IP analysis showing the interaction between LATS2 and UBR5 in SKOV3 cells; (D) Co‐IP analysis showing the interaction between LATS2 and UBR5 in OVCAR‐3 cells; (E) ubiquitination assay measuring LATS2 ubiquitination levels in SKOV3 cells treated with 20 μM GEM for 48 h; (F) ubiquitination assay measuring LATS2 ubiquitination levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (G) WB analysis of in vitro ubiquitination to evaluate UBR5‐mediated LATS2 ubiquitination; (H) WB analysis of Hippo pathway‐related proteins in SKOV3 cells treated with 20 μM GEM for 48 h; (I) WB analysis of Hippo pathway‐related proteins in OVCAR‐3 cells treated with 20 μM GEM for 48 h. Results are presented as mean ± standard deviation. All experiments were repeated three times. *** p < 0.001, using ANOVA and Tukey's multiple comparison test.

Figure Legend Snippet: GEM regulates LATS2 ubiquitination and YAP/TAZ phosphorylation via the hypoxia‐inducible factor 1‐alpha/UBR5 axis. (A) Western blot (WB) analysis of Hippo pathway‐related proteins in SKOV3 cells under hypoxic conditions; (B) WB analysis of Hippo pathway‐related proteins in OVCAR‐3 cells under hypoxic conditions; (C) co‐IP analysis showing the interaction between LATS2 and UBR5 in SKOV3 cells; (D) Co‐IP analysis showing the interaction between LATS2 and UBR5 in OVCAR‐3 cells; (E) ubiquitination assay measuring LATS2 ubiquitination levels in SKOV3 cells treated with 20 μM GEM for 48 h; (F) ubiquitination assay measuring LATS2 ubiquitination levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (G) WB analysis of in vitro ubiquitination to evaluate UBR5‐mediated LATS2 ubiquitination; (H) WB analysis of Hippo pathway‐related proteins in SKOV3 cells treated with 20 μM GEM for 48 h; (I) WB analysis of Hippo pathway‐related proteins in OVCAR‐3 cells treated with 20 μM GEM for 48 h. Results are presented as mean ± standard deviation. All experiments were repeated three times. *** p < 0.001, using ANOVA and Tukey's multiple comparison test.

Techniques Used: Ubiquitin Proteomics, Phospho-proteomics, Western Blot, Co-Immunoprecipitation Assay, In Vitro, Standard Deviation, Comparison

Investigation of GEM's regulation of the Hippo pathway in ovarian cancer inhibition. (A) Western blot (WB) analysis of YAP1 and FGFR1 expression levels in SKOV3 cells treated with 20 μM GEM for 48 h; (B) WB analysis of YAP1 and FGFR1 expression levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (C) CCK8 assay measuring cell viability in SKOV3 cells treated with 20 μM GEM for 48 h; (D) CCK8 assay measuring cell viability in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (E) wound healing assay showing migration rates of SKOV3 cells treated with 20 μM GEM for 48 h (scale bar: 100 μm); (F) wound healing assay showing migration rates of OVCAR‐3 cells treated with 20 μM GEM for 48 h (scale bar: 100 μm); (G) transwell assay showing invasion ability of SKOV3 cells treated with 20 μM GEM for 48 h (scale bar: 50 μm); (H) transwell assay showing invasion ability of OVCAR‐3 cells treated with 20 μM GEM for 48 h (scale bar: 50 μm). Results are presented as mean ± standard deviation. Cell experiments were repeated 3 times; *** p < 0.001, using ANOVA and Tukey's multiple comparison test.

Figure Legend Snippet: Investigation of GEM's regulation of the Hippo pathway in ovarian cancer inhibition. (A) Western blot (WB) analysis of YAP1 and FGFR1 expression levels in SKOV3 cells treated with 20 μM GEM for 48 h; (B) WB analysis of YAP1 and FGFR1 expression levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (C) CCK8 assay measuring cell viability in SKOV3 cells treated with 20 μM GEM for 48 h; (D) CCK8 assay measuring cell viability in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (E) wound healing assay showing migration rates of SKOV3 cells treated with 20 μM GEM for 48 h (scale bar: 100 μm); (F) wound healing assay showing migration rates of OVCAR‐3 cells treated with 20 μM GEM for 48 h (scale bar: 100 μm); (G) transwell assay showing invasion ability of SKOV3 cells treated with 20 μM GEM for 48 h (scale bar: 50 μm); (H) transwell assay showing invasion ability of OVCAR‐3 cells treated with 20 μM GEM for 48 h (scale bar: 50 μm). Results are presented as mean ± standard deviation. Cell experiments were repeated 3 times; *** p < 0.001, using ANOVA and Tukey's multiple comparison test.

Techniques Used: Inhibition, Western Blot, Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Assay, Standard Deviation, Comparison

Cell Culture:

Article Title: Clinical significance and impact on the cell behaviors of miR-758-5p/MMP-2 axis in ovarian cancer cells.
Article Snippet: .. Cell culture and transfection AR TI LE IN PR ES S The human OC cell lines SKOV3, A2780, OVCAR3, COV644, and the normal ovarian epithelial cell line (IOSE cells) were obtained from American Type Culture Collection (ATCC). .. The cells were cultured in DMEM-F12 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin (Thermo Fisher Scientific).

Article Title: Bidirectional Association Between Atrial Fibrillation and Ovarian Cancer: Evidence From the UK Biobank and Mendelian Randomization
Article Snippet: .. P 277 values were calculated using the log-rank test implemented in the Survival package in 278 R. 279 Cell culture 280 D ow nloaded from http://aacrjournals.org/cebp/article-pdf/doi/10.1158/1055-9965.EPI-25-0949/3669634/epi-25-0949.pdf by guest on 16 N ovem ber 2025 17 The human OC cell lines SKOV3 were obtained from the American Type Culture 281 Collection (ATCC, Manassas, VA, USA) and cultured in Dulbecco’s modified 282 Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum (FBS; GIBCO) 283 and 1% penicillin-streptomycin (Hyclone, Logan, Utah, USA), in an incubator at 284 37 °C with 5% CO 2 . ..

Article Title: Integrating necroptosis and immune landscapes: a multi-omics-derived NecropImmScore stratifies prognosis and therapy in ovarian cancer
Article Snippet: .. The human OC cell lines SKOV3 and HEY (both from ATCC, Manassas, VA, USA), the T -cell line Jurkat Clone E6-1 (Procell #CL-0129), and the monocytic cell line THP-1 (ATCC) were cultured in RPMI 1640 (SKOV3, Jurkat, THP-1; Procell) or DMEM (HEY; Procell). .. All media were supplemented with 10% fetal bovine serum (Biological Industries) and 1% penicillin/streptomycin (New Cell & Molecular Biotech), and cells were maintained at 37 °C under 5% CO2.

Transfection:

Modification:

Mutagenesis:

Article Title: Inhibition of LncRNA THUMPD3-AS1 enhances olaparib-induced autophagy in BRCA mutant ovarian cancer cells via PI3K pathway.
Article Snippet: .. Three human OC cell lines SKOV3, SNU-251 (BRCA mutant) and UWB1.289 (BRCA mutant) were provided by American Type Culture Collection (ATCC, Manassas, USA). ..

Image Search Results

Journal: Journal of Cell Communication and Signaling

doi: 10.1002/ccs3.70085

Figure Lengend Snippet: Effects of GEM on hypoxia‐inducible factor 1‐alpha (HIF1A), UBR5, and ovarian cancer Cells. (A) Western blot (WB) analysis of HIF1A and UBR5 expression in SKOV3 cells under hypoxic conditions treated with different concentrations of GEM; (B) WB analysis of HIF1A and UBR5 expression in OVCAR‐3 cells under hypoxic conditions treated with different concentrations of GEM; (C) CCK‐8 assay of cell viability in SKOV3 cells treated with varying concentrations of GEM at 0, 24, and 48 h; (D) CCK‐8 assay of cell viability in OVCAR‐3 cells treated with varying concentrations of GEM at 0, 24, and 48 h; (E) wound healing assay assessing the migration rate of SKOV3 cells treated with different concentrations of GEM at 0 h, 24 h, and 48 h (scale bar: 100 μm); (F) wound healing assay assessing the migration rate of OVCAR‐3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 100 μm); (G) transwell invasion assay evaluating the invasive capacity of SKOV3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 50 μm); (H) transwell invasion assay evaluating the invasive capacity of OVCAR‐3 cells treated with different concentrations of GEM at 0, 24, and 48 h (scale bar: 50 μm). Data are presented as mean ± SD; all cellular experiments were performed in triplicate. *** p < 0.001, analyzed using ANOVA followed by Tukey's multiple comparison test.

Article Snippet: Human OC cell lines SKOV3 (HTB‐77, ATCC) and OVCAR‐3 (HTB‐161, ATCC) were obtained from ATCC.

Techniques: Western Blot, Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Comparison

Journal: Journal of Cell Communication and Signaling

doi: 10.1002/ccs3.70085

Figure Lengend Snippet: Effects of GEM on ovarian cancer proliferation and invasion via HIF1A‐mediated downregulation of UBR5. (A) Western blot (WB) analysis of hypoxia‐inducible factor 1‐alpha (HIF1A) and UBR5 expression levels in SKOV3 cells treated with 20 μM GEM for 48 h; (B) WB analysis of HIF1A and UBR5 expression levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (C) CCK8 assay showing cell viability of SKOV3 cells treated with 20 μM GEM for 48 h; (D) CCK8 assay showing cell viability of OVCAR‐3 cells treated with 20 μM GEM for 48 h; (E) wound healing assay assessing the migration rate of SKOV3 cells treated with 20 μM GEM for 48 h (Scale bar: 100 μm); (F) wound healing assay assessing the migration rate of OVCAR‐3 cells treated with 20 μM GEM for 48 h (Scale bar: 100 μm); (G) transwell invasion assay showing the invasive capacity of SKOV3 cells treated with 20 μM GEM for 48 h (Scale bar: 50 μm); (H) transwell invasion assay showing the invasive capacity of OVCAR‐3 cells treated with 20 μM GEM for 48 h (Scale bar: 50 μm); (I) predicted transcription factor binding sites in the UBR5 promoter region based on JASPAR database analysis; (J) ChIP‐PCR analysis showing HIF1A enrichment at the UBR5 promoter region; (K) dual‐luciferase reporter assay evaluating the regulatory effect of HIF1A on UBR5 promoter activity; (L, M) RT‐qPCR analysis of HIF1A and UBR5 mRNA expression levels after shHIF1A knockdown in SKOV3 and OVCAR‐3 cells; (N, O) RT‐qPCR analysis of UBR5 mRNA expression levels in SKOV3 and OVCAR‐3 cells under normoxia, hypoxia, hypoxia + shNC, and hypoxia + shHIF1A conditions. Data are presented as mean ± SD; all cell experiments were performed in triplicate. *** p < 0.001, analyzed by ANOVA followed by Tukey's multiple comparison test.

Article Snippet: Human OC cell lines SKOV3 (HTB‐77, ATCC) and OVCAR‐3 (HTB‐161, ATCC) were obtained from ATCC.

Techniques: Western Blot, Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Quantitative RT-PCR, Knockdown, Comparison

Journal: Journal of Cell Communication and Signaling

doi: 10.1002/ccs3.70085

Figure Lengend Snippet: GEM regulates LATS2 ubiquitination and YAP/TAZ phosphorylation via the hypoxia‐inducible factor 1‐alpha/UBR5 axis. (A) Western blot (WB) analysis of Hippo pathway‐related proteins in SKOV3 cells under hypoxic conditions; (B) WB analysis of Hippo pathway‐related proteins in OVCAR‐3 cells under hypoxic conditions; (C) co‐IP analysis showing the interaction between LATS2 and UBR5 in SKOV3 cells; (D) Co‐IP analysis showing the interaction between LATS2 and UBR5 in OVCAR‐3 cells; (E) ubiquitination assay measuring LATS2 ubiquitination levels in SKOV3 cells treated with 20 μM GEM for 48 h; (F) ubiquitination assay measuring LATS2 ubiquitination levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (G) WB analysis of in vitro ubiquitination to evaluate UBR5‐mediated LATS2 ubiquitination; (H) WB analysis of Hippo pathway‐related proteins in SKOV3 cells treated with 20 μM GEM for 48 h; (I) WB analysis of Hippo pathway‐related proteins in OVCAR‐3 cells treated with 20 μM GEM for 48 h. Results are presented as mean ± standard deviation. All experiments were repeated three times. *** p < 0.001, using ANOVA and Tukey's multiple comparison test.

Article Snippet: Human OC cell lines SKOV3 (HTB‐77, ATCC) and OVCAR‐3 (HTB‐161, ATCC) were obtained from ATCC.

Techniques: Ubiquitin Proteomics, Phospho-proteomics, Western Blot, Co-Immunoprecipitation Assay, In Vitro, Standard Deviation, Comparison

Journal: Journal of Cell Communication and Signaling

doi: 10.1002/ccs3.70085

Figure Lengend Snippet: Investigation of GEM's regulation of the Hippo pathway in ovarian cancer inhibition. (A) Western blot (WB) analysis of YAP1 and FGFR1 expression levels in SKOV3 cells treated with 20 μM GEM for 48 h; (B) WB analysis of YAP1 and FGFR1 expression levels in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (C) CCK8 assay measuring cell viability in SKOV3 cells treated with 20 μM GEM for 48 h; (D) CCK8 assay measuring cell viability in OVCAR‐3 cells treated with 20 μM GEM for 48 h; (E) wound healing assay showing migration rates of SKOV3 cells treated with 20 μM GEM for 48 h (scale bar: 100 μm); (F) wound healing assay showing migration rates of OVCAR‐3 cells treated with 20 μM GEM for 48 h (scale bar: 100 μm); (G) transwell assay showing invasion ability of SKOV3 cells treated with 20 μM GEM for 48 h (scale bar: 50 μm); (H) transwell assay showing invasion ability of OVCAR‐3 cells treated with 20 μM GEM for 48 h (scale bar: 50 μm). Results are presented as mean ± standard deviation. Cell experiments were repeated 3 times; *** p < 0.001, using ANOVA and Tukey's multiple comparison test.

Article Snippet: Human OC cell lines SKOV3 (HTB‐77, ATCC) and OVCAR‐3 (HTB‐161, ATCC) were obtained from ATCC.

Techniques: Inhibition, Western Blot, Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Assay, Standard Deviation, Comparison

A – D CCK8 assay to assess the effect of UHRF1-knockdown and UHRF1-overexpressed OC cell lines on the proliferation. E EDU cell proliferation assay showing the effect of UHRF1-knockdown OC cell lines. F Colony formation assay showing the effect of UHRF1-knockdown OC cell lines on colony-forming ability. G , H Transwell migration and invasion assays showing the effect of UHRF1-knockdown OC cell lines on migration and invasion abilities. I Wound healing assay showing UHRF1-knockdown SKOV3 cell lines migration. J Tumorigenicity assay in nude mice showing the effect of UHRF1-knockdown SKOV3 cell lines on tumor formation. K Ki67 staining of tumor tissues to assess the effect of UHRF1 knockdown on cell proliferation. ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Journal: Cell Death & Disease

Article Title: UHRF1-mediated HIF-1α stabilization promotes ovarian cancer through metabolic reprogramming and angiogenesis

doi: 10.1038/s41419-025-08033-w

Figure Lengend Snippet: A – D CCK8 assay to assess the effect of UHRF1-knockdown and UHRF1-overexpressed OC cell lines on the proliferation. E EDU cell proliferation assay showing the effect of UHRF1-knockdown OC cell lines. F Colony formation assay showing the effect of UHRF1-knockdown OC cell lines on colony-forming ability. G , H Transwell migration and invasion assays showing the effect of UHRF1-knockdown OC cell lines on migration and invasion abilities. I Wound healing assay showing UHRF1-knockdown SKOV3 cell lines migration. J Tumorigenicity assay in nude mice showing the effect of UHRF1-knockdown SKOV3 cell lines on tumor formation. K Ki67 staining of tumor tissues to assess the effect of UHRF1 knockdown on cell proliferation. ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: The human OC cell line SKOV3 (CL-0215) was purchased from Wuhan Procell Life Science & Technology Co., Ltd., and A2780 (STCC10706P-1) was purchased from Wuhan Servicebio Technology Co., Ltd.

Techniques: CCK-8 Assay, Knockdown, Proliferation Assay, Colony Assay, Migration, Wound Healing Assay, Tumorigenicity Assay, Staining

A Volcano plot showing differential expression analysis between sh-NC SKOV3 cells and sh-UHRF1#2 SKOV3 cells, highlighting key potential downstream molecules. B Heatmap displaying the expression of HIF-1 signaling pathway genes between the knockdown and control groups. C , D KEGG pathway enrichment analysis of differentially expressed genes (DEGs), bubble chart shows the enriched pathways; circle plot displays the specific genes within the pathways. E GO-MF enrichment analysis of DEGs, the specific pathway names can be found in (Supplementary Table ). F GSEA enrichment analysis of DEGs. G Correlation analysis of UHRF1 and HIF-1 signaling pathway genes using GEPIA2.

Journal: Cell Death & Disease

Article Title: UHRF1-mediated HIF-1α stabilization promotes ovarian cancer through metabolic reprogramming and angiogenesis

doi: 10.1038/s41419-025-08033-w

Figure Lengend Snippet: A Volcano plot showing differential expression analysis between sh-NC SKOV3 cells and sh-UHRF1#2 SKOV3 cells, highlighting key potential downstream molecules. B Heatmap displaying the expression of HIF-1 signaling pathway genes between the knockdown and control groups. C , D KEGG pathway enrichment analysis of differentially expressed genes (DEGs), bubble chart shows the enriched pathways; circle plot displays the specific genes within the pathways. E GO-MF enrichment analysis of DEGs, the specific pathway names can be found in (Supplementary Table ). F GSEA enrichment analysis of DEGs. G Correlation analysis of UHRF1 and HIF-1 signaling pathway genes using GEPIA2.

Techniques: Quantitative Proteomics, Expressing, Knockdown, Control

A Tissue immunofluorescence (IF) confirmed the colocalization of UHRF1 and HIF-1α in tissues. B Silver staining of mass spectrometry samples. C Co-immunoprecipitation (co-IP) confirmed the interaction between UHRF1 and HIF-1α in SKOV3 cells. D Forward and reverse co-IP validated the interaction between UHRF1 and HIF-1α in 293T cells. E IB analysis of interaction domains between HIF-1α and UHRF1 using truncated plasmids co-transfected in 293T cells. F Truncated sequence map of UHRF1. G Truncated sequence map of HIF-1α. H WB analysis of interaction domains between UHRF1 and HIF-1α using truncated plasmids co-transfected in 293T cells. I WB analysis of UHRF1’s effect on the nuclear translocation of HIF-1α. J IF analysis of UHRF1’s effect on HIF-1α nuclear translocation.

Journal: Cell Death & Disease

Article Title: UHRF1-mediated HIF-1α stabilization promotes ovarian cancer through metabolic reprogramming and angiogenesis

doi: 10.1038/s41419-025-08033-w

Figure Lengend Snippet: A Tissue immunofluorescence (IF) confirmed the colocalization of UHRF1 and HIF-1α in tissues. B Silver staining of mass spectrometry samples. C Co-immunoprecipitation (co-IP) confirmed the interaction between UHRF1 and HIF-1α in SKOV3 cells. D Forward and reverse co-IP validated the interaction between UHRF1 and HIF-1α in 293T cells. E IB analysis of interaction domains between HIF-1α and UHRF1 using truncated plasmids co-transfected in 293T cells. F Truncated sequence map of UHRF1. G Truncated sequence map of HIF-1α. H WB analysis of interaction domains between UHRF1 and HIF-1α using truncated plasmids co-transfected in 293T cells. I WB analysis of UHRF1’s effect on the nuclear translocation of HIF-1α. J IF analysis of UHRF1’s effect on HIF-1α nuclear translocation.

Techniques: Immunofluorescence, Silver Staining, Mass Spectrometry, Immunoprecipitation, Co-Immunoprecipitation Assay, Transfection, Sequencing, Translocation Assay

A UMAP plot with clusters demarcated by colors demonstrating 12 distinct clusters based on gene expression differences for epithelial cells passing quality control. B The UMAP plot demarcated by colors showing the two groups of OC tumors (malignant) and nonmalignant ovarian tissues. C Expression of HIF signaling pathway genes in tumor and normal tissues. D Expression of HIF signaling pathway genes in each epithelial cell cluster. E UMAP plot color coded for the expression (blue to purple) of marker genes for HIF signaling pathway genes. F The proportion of epithelial cell types relative to the total epithelial cell count in each clinical patient. G KEGG pathway enrichment analysis of epithelial-cluster6 genes. H , I UHRF1-knockout and UHRF1-overexpressed SKOV3 cell lines were treated with CoCl₂ for 24 h, and WB analysis was performed to assess the expression levels of glycolysis-related proteins. J – M UHRF1-knockdown and UHRF1-overexpressed OC cell lines were cultured under normoxic and hypoxic conditions for 48 h, and glucose consumption and lactate production were measured. Data are presented as mean ± SD from three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Journal: Cell Death & Disease

Article Title: UHRF1-mediated HIF-1α stabilization promotes ovarian cancer through metabolic reprogramming and angiogenesis

doi: 10.1038/s41419-025-08033-w

Figure Lengend Snippet: A UMAP plot with clusters demarcated by colors demonstrating 12 distinct clusters based on gene expression differences for epithelial cells passing quality control. B The UMAP plot demarcated by colors showing the two groups of OC tumors (malignant) and nonmalignant ovarian tissues. C Expression of HIF signaling pathway genes in tumor and normal tissues. D Expression of HIF signaling pathway genes in each epithelial cell cluster. E UMAP plot color coded for the expression (blue to purple) of marker genes for HIF signaling pathway genes. F The proportion of epithelial cell types relative to the total epithelial cell count in each clinical patient. G KEGG pathway enrichment analysis of epithelial-cluster6 genes. H , I UHRF1-knockout and UHRF1-overexpressed SKOV3 cell lines were treated with CoCl₂ for 24 h, and WB analysis was performed to assess the expression levels of glycolysis-related proteins. J – M UHRF1-knockdown and UHRF1-overexpressed OC cell lines were cultured under normoxic and hypoxic conditions for 48 h, and glucose consumption and lactate production were measured. Data are presented as mean ± SD from three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques: Gene Expression, Control, Expressing, Marker, Cell Counting, Knock-Out, Knockdown, Cell Culture

A , B Periodic acid-Schiff (PAS) (pink) and CD31 (brown) double staining of tumor tissues from xenograft mice. PAS+/CD31+ tubular structures represent conventional blood vessels lined with CD31-positive endothelial cells. Adjacent PAS+/CD31− tubular structures suggest vasculogenic mimicry (VM). C , D WB analysis of VEGF expression levels in cells treated with CoCl₂ for 24 h. E Representative images of the tube formation assay in SKOV3 stable cell lines. F Representative images of the tube formation assay in HUVEC cells after 72 h of culture with conditioned medium from the stable SKOV3 cell line. G Images of the Transwell migration assay and tube formation assay in HUVEC cells after 72 hours of culture with conditioned medium from the stable SKOV3 cell line. H , I Images of the Transwell migration assay and tube formation assay in HUVEC cells after 72 h of culture with conditioned medium from the stable SKOV3 cell line, followed by treatment with the HIF-1α inhibitor PX-478. J , K IC50 analysis of Bevacizumab in UHRF1-knockdown A2780 cell lines. ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Journal: Cell Death & Disease

Article Title: UHRF1-mediated HIF-1α stabilization promotes ovarian cancer through metabolic reprogramming and angiogenesis

doi: 10.1038/s41419-025-08033-w

Figure Lengend Snippet: A , B Periodic acid-Schiff (PAS) (pink) and CD31 (brown) double staining of tumor tissues from xenograft mice. PAS+/CD31+ tubular structures represent conventional blood vessels lined with CD31-positive endothelial cells. Adjacent PAS+/CD31− tubular structures suggest vasculogenic mimicry (VM). C , D WB analysis of VEGF expression levels in cells treated with CoCl₂ for 24 h. E Representative images of the tube formation assay in SKOV3 stable cell lines. F Representative images of the tube formation assay in HUVEC cells after 72 h of culture with conditioned medium from the stable SKOV3 cell line. G Images of the Transwell migration assay and tube formation assay in HUVEC cells after 72 hours of culture with conditioned medium from the stable SKOV3 cell line. H , I Images of the Transwell migration assay and tube formation assay in HUVEC cells after 72 h of culture with conditioned medium from the stable SKOV3 cell line, followed by treatment with the HIF-1α inhibitor PX-478. J , K IC50 analysis of Bevacizumab in UHRF1-knockdown A2780 cell lines. ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Techniques: Double Staining, Expressing, Tube Formation Assay, Stable Transfection, Transwell Migration Assay, Knockdown

Review

human oc cell lines skov3 (ATCC)

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1) Product Images from "Gemcitabine activates the Hippo signaling pathway and suppresses tumor growth by stabilizing large tumor suppressor kinase 2 through the hypoxia‐inducible factor 1‐alpha/ubiquitin protein ligase E3 component N‐recognin 5 axis"

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