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human ovarian cancer cell line skov3  (ATCC)


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    ATCC human ovarian cancer cell line skov3
    Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – <t>SKOV3</t> tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.
    Human Ovarian Cancer Cell Line Skov3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7636 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sk+ov/SK-OV-3/pmc13084341-20-13-22
    Average 99 stars, based on 7636 article reviews
    human ovarian cancer cell line skov3 - by Bioz Stars, 2026-09
    99/100 stars

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    1) Product Images from "Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example"

    Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

    Journal: Genes & Diseases

    doi: 10.1016/j.gendis.2025.101978

    Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.
    Figure Legend Snippet: Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Techniques Used: Transduction, Control, Incubation, Enzyme-linked Immunosorbent Assay, Standard Deviation

    TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.
    Figure Legend Snippet: TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

    Techniques Used: Activity Assay, In Vivo, Expressing, Luciferase, In Vivo Imaging

    Related Articles

    Inhibition:

    Article Title: Thienopyranones and furanopyranones as kinase, bromodomain, and checkpoint inhibitors
    Article Snippet: .. The individual cell line growth percent inhibition for compound 1 is listed below grouped by cancer type: Leukemia CCRF-CEM −14.44 HL-60(TB) −46.74 K-562 2.96 MOLT-4 −31.97 RPMI-8226 −46.71 SR 0.02 Non-Small Cell Lung Cancer A549/ATCC −36.82 EKVX −19.52 HOP-62 −30.36 HOP-92 −3.68 NCI-H226 2.17 NCI-H23 −10.23 NCI-H322M −28.97 NCI-H460 −26.41 NCI-H522 −65.10 Colon Cancer COLO 205 −84.28 HCC-2998 −44.57 HCT-116 −29.20 HCT-15 −11.42 HT29 −48.56 KM12 −86.90 SW-620 −45.59 CNS Cancer SF-268 −2.94 SF-295 −36.90 SF-539 −70.17 SNB-19 1.45 SNB-75 −65.05 U251 −7.84 Melanoma LOX IMVI −39.35 MALME-3M −67.87 M14 −73.37 MDA-MB-435 −38.71 SK-MEL-2 −58.60 SK-MEL-28 −55.86 SK-MEL-5 −98.03 UACC-257 −81.54 UACC-62 −69.59 Ovarian Cancer IGROV1 −7.11 OVCAR-3 2.63 OVCAR-4 12.39 OVCAR-5 −9.43 OVCAR-8 2.54 NCI/ADR-RES 0.63 SK-OV-3 −28.34 Renal Cancer 786-0 −1.22 ACHN 1.06 CAKI-1 −50.83 RXF 393 −85.84 SN12C 4.35 TK-10 −10.03 UO-31 −5.39 Prostate Cancer PC-3 −42.03 DU-145 −97.13 Breast Cancer MCF7 −46.81 MDA-MB-231/ATCC −7.21 HS 578T −8.99 BT-549 −79.13 T-47D −4.72 MDA-MB-468 −5.41 ..

    Multiple Displacement Amplification:

    Article Title: Thienopyranones and furanopyranones as kinase, bromodomain, and checkpoint inhibitors
    Article Snippet: .. The individual cell line growth percent inhibition for compound 1 is listed below grouped by cancer type: Leukemia CCRF-CEM −14.44 HL-60(TB) −46.74 K-562 2.96 MOLT-4 −31.97 RPMI-8226 −46.71 SR 0.02 Non-Small Cell Lung Cancer A549/ATCC −36.82 EKVX −19.52 HOP-62 −30.36 HOP-92 −3.68 NCI-H226 2.17 NCI-H23 −10.23 NCI-H322M −28.97 NCI-H460 −26.41 NCI-H522 −65.10 Colon Cancer COLO 205 −84.28 HCC-2998 −44.57 HCT-116 −29.20 HCT-15 −11.42 HT29 −48.56 KM12 −86.90 SW-620 −45.59 CNS Cancer SF-268 −2.94 SF-295 −36.90 SF-539 −70.17 SNB-19 1.45 SNB-75 −65.05 U251 −7.84 Melanoma LOX IMVI −39.35 MALME-3M −67.87 M14 −73.37 MDA-MB-435 −38.71 SK-MEL-2 −58.60 SK-MEL-28 −55.86 SK-MEL-5 −98.03 UACC-257 −81.54 UACC-62 −69.59 Ovarian Cancer IGROV1 −7.11 OVCAR-3 2.63 OVCAR-4 12.39 OVCAR-5 −9.43 OVCAR-8 2.54 NCI/ADR-RES 0.63 SK-OV-3 −28.34 Renal Cancer 786-0 −1.22 ACHN 1.06 CAKI-1 −50.83 RXF 393 −85.84 SN12C 4.35 TK-10 −10.03 UO-31 −5.39 Prostate Cancer PC-3 −42.03 DU-145 −97.13 Breast Cancer MCF7 −46.81 MDA-MB-231/ATCC −7.21 HS 578T −8.99 BT-549 −79.13 T-47D −4.72 MDA-MB-468 −5.41 ..

    Article Title: Substituted [1,2,4]triazolo[4,3-c]pyrimidines that induce degradation of embryonic ectoderm development (EED) protein
    Article Snippet: .. The disclosed compounds and PROTACs may be effective in inhibiting cell proliferation of one or more types of cancer cells including: multiple myeloma cells, such as MM.1S cells; leukemia cells, such as CCRF-CEM, HL-60(TB), MOLT-4, RPMI-8226 and SR; non-small lung cancer cells, such as A549/ATCC, EKVX, HOP-62, HOP-92, NCI-H226, NCI-H23, NCI-H322M, NCI-H460 and NCI-H522; colon cancer cells, such as COLO 205, HCC-2998, HCT-116, HCT-15, HT29, KM12 and SW-620; CNS: SF-268, SF-295, SF-539, SNB-19, SNB-75 and U251; melanoma cancer cells, such as LOX IMVI, MALME-3M, M14, MDA-MB-435, SK-MEL-2, SK-MEL-28, SK-MEL-5, UACC-257 and UACC-62; ovarian cancer cells, such as IGR-OV1, OVCAR-3, OVCAR-4, OVCAR-5, OVCAR-8, NCI/ADR-RES and SK-OV-3; renal cancer cells, such as 786-0, A498, ACHN, CAKI-1, RXF 393, SN12C, TK-10 and UO-31; prostate cancer cells, such as DU-145 and PC-3; and breast cancer cells, such as MCF7, MDA-MB-231/ATCC, MDA-MB-468, HS 578T, BT-549 and T-47D. ..

    Cell Culture:

    Article Title: An Octopus probe for high-performance >1,300 nm NIR-II fluorescence molecular imaging of cancer.
    Article Snippet: Precise intraoperative tumor resection is critical for cancer treatment but remains challenging.. We developed “Octopus” (OCTP), a modular NIR-II (>1,300 nm) probe targeting folate receptor.. Compared to clinical probe Cytalux, OCTP exhibits superior tumor-to-background ratios and mean tumor fluorescence intensity via multi-arm PEG design.

    Article Title: Dysregulated BARD1 Contributes to Paclitaxel Resistance in Ovarian Cancer via Up-regulating CYP2C8.
    Article Snippet: .. Human OC cell lines CaoV-3 and SK-OV-3 were purchased from the American Type Culture Collection (ATCC) and cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) containing 10 % foetal bovine serum (Hyclone, Logan, UT), 100 IU/ml penicillin and 100 IU/ml streptomycin. ..

    Article Title: Selection and evaluation of new sites for splitting beta-lactamase to modulate auto-complementation enzyme activity
    Article Snippet: NCI-N87 were cultured in RPMI 1640 medium (ATCC modification, Gibco TM Cat# 11875093) supplemented with 10 % FBS and 1× Antibiotic-Antimycotic solution. .. SK-OV-3 were cultured in McCoy’s (ATCC modification, Gibco TM Cat# 16600082) supplemented with 10 % FBS and 1× Antibiotic-Antimycotic solution. ..

    Article Title: Integrated single-cell and bulk transcriptomics reveals STAB1 as a novel therapeutic target for ovarian cancer.
    Article Snippet: .. Key ligand-receptor interactions mediating macrophage-tumor crosstalk were visualized using chord diagrams and hierarchy plots Cell culture and siRNA knockdown Human OC cell lines A2780 and SK-OV-3 were obtained from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium supplemented with 10 % fetal bovine serum (FBS), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 ◦C in 5 % CO2. .. STAB1targeted small interfering RNA (si-STAB1) and non-targeting control siRNA (si-NC) were synthesized by GenePharma (Shanghai, China) and transfected using Lipofectamine 3000 (Invitrogen) according to the manufacturer's protocol (final concentration: 50 nM).

    Article Title: Integrated single-cell and bulk transcriptomics reveals STAB1 as a novel therapeutic target for ovarian cancer
    Article Snippet: .. Human OC cell lines A2780 and SK-OV-3 were obtained from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium supplemented with 10 % fetal bovine serum (FBS), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 °C in 5 % CO2. .. STAB1-targeted small interfering RNA (si-STAB1) and non-targeting control siRNA (si-NC) were synthesized by GenePharma (Shanghai, China) and transfected using Lipofectamine 3000 (Invitrogen) according to the manufacturer's protocol (final concentration: 50 nM).

    Article Title: FGFR1 suppresses ovarian cancer progression by modulating SIRT3-dependent lactylation and metabolic reprogramming.
    Article Snippet: .. Cell Culture and Transfection Procedures Human OC cell lines OVCAR-3 and SK-OV-3 were sourced from the American Type Culture Collection. .. The cells were cultured in RPMI 1640 medium (Gibco, USA) supplemented with 1% antibiotics (100 μg/mL penicillin G and 100 μg/mL streptomycin, Gibco, USA) and 10% FBS (Gibco, USA) under standard conditions (37°C, 5%CO2).

    Modification:

    Article Title: Dysregulated BARD1 Contributes to Paclitaxel Resistance in Ovarian Cancer via Up-regulating CYP2C8.
    Article Snippet: .. Human OC cell lines CaoV-3 and SK-OV-3 were purchased from the American Type Culture Collection (ATCC) and cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) containing 10 % foetal bovine serum (Hyclone, Logan, UT), 100 IU/ml penicillin and 100 IU/ml streptomycin. ..

    Article Title: Selection and evaluation of new sites for splitting beta-lactamase to modulate auto-complementation enzyme activity
    Article Snippet: NCI-N87 were cultured in RPMI 1640 medium (ATCC modification, Gibco TM Cat# 11875093) supplemented with 10 % FBS and 1× Antibiotic-Antimycotic solution. .. SK-OV-3 were cultured in McCoy’s (ATCC modification, Gibco TM Cat# 16600082) supplemented with 10 % FBS and 1× Antibiotic-Antimycotic solution. ..

    Knockdown:

    Article Title: Integrated single-cell and bulk transcriptomics reveals STAB1 as a novel therapeutic target for ovarian cancer.
    Article Snippet: .. Key ligand-receptor interactions mediating macrophage-tumor crosstalk were visualized using chord diagrams and hierarchy plots Cell culture and siRNA knockdown Human OC cell lines A2780 and SK-OV-3 were obtained from the American Type Culture Collection (ATCC) and cultured in RPMI-1640 medium supplemented with 10 % fetal bovine serum (FBS), 100 U/mL penicillin, and 100 μg/mL streptomycin at 37 ◦C in 5 % CO2. .. STAB1targeted small interfering RNA (si-STAB1) and non-targeting control siRNA (si-NC) were synthesized by GenePharma (Shanghai, China) and transfected using Lipofectamine 3000 (Invitrogen) according to the manufacturer's protocol (final concentration: 50 nM).

    Transfection:

    Article Title: FGFR1 suppresses ovarian cancer progression by modulating SIRT3-dependent lactylation and metabolic reprogramming.
    Article Snippet: .. Cell Culture and Transfection Procedures Human OC cell lines OVCAR-3 and SK-OV-3 were sourced from the American Type Culture Collection. .. The cells were cultured in RPMI 1640 medium (Gibco, USA) supplemented with 1% antibiotics (100 μg/mL penicillin G and 100 μg/mL streptomycin, Gibco, USA) and 10% FBS (Gibco, USA) under standard conditions (37°C, 5%CO2).



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    Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

    doi: 10.1016/j.gendis.2025.101978

    Figure Lengend Snippet: Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

    Techniques: Transduction, Control, Incubation, Enzyme-linked Immunosorbent Assay, Standard Deviation

    TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

    Journal: Genes & Diseases

    Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

    doi: 10.1016/j.gendis.2025.101978

    Figure Lengend Snippet: TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

    Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

    Techniques: Activity Assay, In Vivo, Expressing, Luciferase, In Vivo Imaging

    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.

    Journal: Journal of Cell Communication and Signaling

    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

    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

    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.

    Journal: Journal of Cell Communication and Signaling

    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

    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

    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.

    Journal: Journal of Cell Communication and Signaling

    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

    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

    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.

    Journal: Journal of Cell Communication and Signaling

    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

    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