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human ovarian cancer cell line skov3  (ATCC)


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    Structured Review

    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 7540 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 7540 article reviews
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    Images

    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



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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.
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    ATCC ov cell lines
    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.
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    ATCC hgsoc cell lines sk ov 3
    Genome-wide landscape and locus-specific analyses of EOC GWAS signals. Manhattan plots of subtype-specific GWAS signals in EOC from the Dareng et al. (A) and Phelan et al. (B) studies. In each panel, Manhattan plots are ordered from top to bottom for <t>HGSOC,</t> LGSOC, ENOC, OCCC, and MOC. The horizontal dashed line denotes the genome-wide significance threshold ( P < 5 × 10⁻⁸). (C) Cross-cohort genetic landscape. Circos plot displays lead risk loci and mapped genes from the Dareng et al. (inner ring) and Phelan et al. (middle ring) GWAS. Colors represent EOC subtypes. The outer ring shows chromosome ideograms. For each subtype, the top five genes, selected by a multi-step prioritization ( P < 1 × 10⁻⁵ and pLI > 0.9), are labeled. Cross-subtype genes are highlighted in black. (D) Upset plot showing the number of genome-wide significant lead risk loci identified by FUMA across cohorts and EOC subtypes. (E) Regional association plot for HGSOC on chromosome 22. The -log 10 ( P- value) for each SNP (left Y-axis) is plotted against chromosomal position (X-axis); points are colored by pairwise LD (r²) with lead SNP rs6005807 (1000 Genomes EUR, EUR panel). Annotated genes are shown below. (F) LocusCompare plot illustrating colocalization between GWAS and cis-pQTL signals around rs6005807. Each point represents an SNP, with –log 10 ( P- value) for GWAS on the X-axis and for cis-pQTL on the Y-axis; points are colored by LD (r²) with the lead SNP.
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    ATCC human breast cancer cell lines skov3
    Genome-wide landscape and locus-specific analyses of EOC GWAS signals. Manhattan plots of subtype-specific GWAS signals in EOC from the Dareng et al. (A) and Phelan et al. (B) studies. In each panel, Manhattan plots are ordered from top to bottom for <t>HGSOC,</t> LGSOC, ENOC, OCCC, and MOC. The horizontal dashed line denotes the genome-wide significance threshold ( P < 5 × 10⁻⁸). (C) Cross-cohort genetic landscape. Circos plot displays lead risk loci and mapped genes from the Dareng et al. (inner ring) and Phelan et al. (middle ring) GWAS. Colors represent EOC subtypes. The outer ring shows chromosome ideograms. For each subtype, the top five genes, selected by a multi-step prioritization ( P < 1 × 10⁻⁵ and pLI > 0.9), are labeled. Cross-subtype genes are highlighted in black. (D) Upset plot showing the number of genome-wide significant lead risk loci identified by FUMA across cohorts and EOC subtypes. (E) Regional association plot for HGSOC on chromosome 22. The -log 10 ( P- value) for each SNP (left Y-axis) is plotted against chromosomal position (X-axis); points are colored by pairwise LD (r²) with lead SNP rs6005807 (1000 Genomes EUR, EUR panel). Annotated genes are shown below. (F) LocusCompare plot illustrating colocalization between GWAS and cis-pQTL signals around rs6005807. Each point represents an SNP, with –log 10 ( P- value) for GWAS on the X-axis and for cis-pQTL on the Y-axis; points are colored by LD (r²) with the lead SNP.
    Human Breast Cancer Cell Lines Skov3, 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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    ATCC human oc cell lines
    Genome-wide landscape and locus-specific analyses of EOC GWAS signals. Manhattan plots of subtype-specific GWAS signals in EOC from the Dareng et al. (A) and Phelan et al. (B) studies. In each panel, Manhattan plots are ordered from top to bottom for <t>HGSOC,</t> LGSOC, ENOC, OCCC, and MOC. The horizontal dashed line denotes the genome-wide significance threshold ( P < 5 × 10⁻⁸). (C) Cross-cohort genetic landscape. Circos plot displays lead risk loci and mapped genes from the Dareng et al. (inner ring) and Phelan et al. (middle ring) GWAS. Colors represent EOC subtypes. The outer ring shows chromosome ideograms. For each subtype, the top five genes, selected by a multi-step prioritization ( P < 1 × 10⁻⁵ and pLI > 0.9), are labeled. Cross-subtype genes are highlighted in black. (D) Upset plot showing the number of genome-wide significant lead risk loci identified by FUMA across cohorts and EOC subtypes. (E) Regional association plot for HGSOC on chromosome 22. The -log 10 ( P- value) for each SNP (left Y-axis) is plotted against chromosomal position (X-axis); points are colored by pairwise LD (r²) with lead SNP rs6005807 (1000 Genomes EUR, EUR panel). Annotated genes are shown below. (F) LocusCompare plot illustrating colocalization between GWAS and cis-pQTL signals around rs6005807. Each point represents an SNP, with –log 10 ( P- value) for GWAS on the X-axis and for cis-pQTL on the Y-axis; points are colored by LD (r²) with the lead SNP.
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    ATCC ovarian cancer cell line ov90
    Genome-wide landscape and locus-specific analyses of EOC GWAS signals. Manhattan plots of subtype-specific GWAS signals in EOC from the Dareng et al. (A) and Phelan et al. (B) studies. In each panel, Manhattan plots are ordered from top to bottom for <t>HGSOC,</t> LGSOC, ENOC, OCCC, and MOC. The horizontal dashed line denotes the genome-wide significance threshold ( P < 5 × 10⁻⁸). (C) Cross-cohort genetic landscape. Circos plot displays lead risk loci and mapped genes from the Dareng et al. (inner ring) and Phelan et al. (middle ring) GWAS. Colors represent EOC subtypes. The outer ring shows chromosome ideograms. For each subtype, the top five genes, selected by a multi-step prioritization ( P < 1 × 10⁻⁵ and pLI > 0.9), are labeled. Cross-subtype genes are highlighted in black. (D) Upset plot showing the number of genome-wide significant lead risk loci identified by FUMA across cohorts and EOC subtypes. (E) Regional association plot for HGSOC on chromosome 22. The -log 10 ( P- value) for each SNP (left Y-axis) is plotted against chromosomal position (X-axis); points are colored by pairwise LD (r²) with lead SNP rs6005807 (1000 Genomes EUR, EUR panel). Annotated genes are shown below. (F) LocusCompare plot illustrating colocalization between GWAS and cis-pQTL signals around rs6005807. Each point represents an SNP, with –log 10 ( P- value) for GWAS on the X-axis and for cis-pQTL on the Y-axis; points are colored by LD (r²) with the lead SNP.
    Ovarian Cancer Cell Line Ov90, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human epithelial ovarian cancer eoc cell lines sk ov 3
    (A) Schematic representation of hsa-miR-15a and MTX-5-FU-Gem-miR-15a, showing incorporation of 5-fluorouracil and gemcitabine into the miR-15a backbone and conjugation of methotrexate (MTX) to the passenger strand. (B-E) Dose-response curves showing cell viability following treatment with MTX-5-FU-Gem-miR-15a, unmodified miR-15a, and <t>olaparib</t> <t>in</t> <t>SK-OV-3</t> (B), OVCAR-3 (C), A2780 (D), and UWB1.289 (E) cells. Data represent mean ± SD from n = 4 biological replicates.
    Human Epithelial Ovarian Cancer Eoc Cell Lines Sk Ov 3, 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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    ATCC ovarian cancer cell lines skov 3
    (A) Schematic representation of hsa-miR-15a and MTX-5-FU-Gem-miR-15a, showing incorporation of 5-fluorouracil and gemcitabine into the miR-15a backbone and conjugation of methotrexate (MTX) to the passenger strand. (B-E) Dose-response curves showing cell viability following treatment with MTX-5-FU-Gem-miR-15a, unmodified miR-15a, and <t>olaparib</t> <t>in</t> <t>SK-OV-3</t> (B), OVCAR-3 (C), A2780 (D), and UWB1.289 (E) cells. Data represent mean ± SD from n = 4 biological replicates.
    Ovarian Cancer Cell Lines Skov 3, 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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    ATCC transfection procedures human oc cell lines ovcar 3
    (A) Schematic representation of hsa-miR-15a and MTX-5-FU-Gem-miR-15a, showing incorporation of 5-fluorouracil and gemcitabine into the miR-15a backbone and conjugation of methotrexate (MTX) to the passenger strand. (B-E) Dose-response curves showing cell viability following treatment with MTX-5-FU-Gem-miR-15a, unmodified miR-15a, and <t>olaparib</t> <t>in</t> <t>SK-OV-3</t> (B), OVCAR-3 (C), A2780 (D), and UWB1.289 (E) cells. Data represent mean ± SD from n = 4 biological replicates.
    Transfection Procedures Human Oc Cell Lines Ovcar 3, 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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    ATCC ovarian cancer cell line skov3
    Higher expression of CDK9 was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of <t>SKOV3</t> and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.
    Ovarian Cancer Cell Line Skov3, 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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    Image Search Results


    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

    Genome-wide landscape and locus-specific analyses of EOC GWAS signals. Manhattan plots of subtype-specific GWAS signals in EOC from the Dareng et al. (A) and Phelan et al. (B) studies. In each panel, Manhattan plots are ordered from top to bottom for HGSOC, LGSOC, ENOC, OCCC, and MOC. The horizontal dashed line denotes the genome-wide significance threshold ( P < 5 × 10⁻⁸). (C) Cross-cohort genetic landscape. Circos plot displays lead risk loci and mapped genes from the Dareng et al. (inner ring) and Phelan et al. (middle ring) GWAS. Colors represent EOC subtypes. The outer ring shows chromosome ideograms. For each subtype, the top five genes, selected by a multi-step prioritization ( P < 1 × 10⁻⁵ and pLI > 0.9), are labeled. Cross-subtype genes are highlighted in black. (D) Upset plot showing the number of genome-wide significant lead risk loci identified by FUMA across cohorts and EOC subtypes. (E) Regional association plot for HGSOC on chromosome 22. The -log 10 ( P- value) for each SNP (left Y-axis) is plotted against chromosomal position (X-axis); points are colored by pairwise LD (r²) with lead SNP rs6005807 (1000 Genomes EUR, EUR panel). Annotated genes are shown below. (F) LocusCompare plot illustrating colocalization between GWAS and cis-pQTL signals around rs6005807. Each point represents an SNP, with –log 10 ( P- value) for GWAS on the X-axis and for cis-pQTL on the Y-axis; points are colored by LD (r²) with the lead SNP.

    Journal: Translational Oncology

    Article Title: Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining

    doi: 10.1016/j.tranon.2026.102748

    Figure Lengend Snippet: Genome-wide landscape and locus-specific analyses of EOC GWAS signals. Manhattan plots of subtype-specific GWAS signals in EOC from the Dareng et al. (A) and Phelan et al. (B) studies. In each panel, Manhattan plots are ordered from top to bottom for HGSOC, LGSOC, ENOC, OCCC, and MOC. The horizontal dashed line denotes the genome-wide significance threshold ( P < 5 × 10⁻⁸). (C) Cross-cohort genetic landscape. Circos plot displays lead risk loci and mapped genes from the Dareng et al. (inner ring) and Phelan et al. (middle ring) GWAS. Colors represent EOC subtypes. The outer ring shows chromosome ideograms. For each subtype, the top five genes, selected by a multi-step prioritization ( P < 1 × 10⁻⁵ and pLI > 0.9), are labeled. Cross-subtype genes are highlighted in black. (D) Upset plot showing the number of genome-wide significant lead risk loci identified by FUMA across cohorts and EOC subtypes. (E) Regional association plot for HGSOC on chromosome 22. The -log 10 ( P- value) for each SNP (left Y-axis) is plotted against chromosomal position (X-axis); points are colored by pairwise LD (r²) with lead SNP rs6005807 (1000 Genomes EUR, EUR panel). Annotated genes are shown below. (F) LocusCompare plot illustrating colocalization between GWAS and cis-pQTL signals around rs6005807. Each point represents an SNP, with –log 10 ( P- value) for GWAS on the X-axis and for cis-pQTL on the Y-axis; points are colored by LD (r²) with the lead SNP.

    Article Snippet: The HGSOC cell lines SK-OV-3 (ATCC® HTB-77TM) and OVCAR-3 (ATCC® HTB-161TM), as well as the human monocytic cell line THP-1 (ATCC® TIB-202TM), were obtained from the American Type Culture Collection and cultured under standard conditions at 37 °C with 5% CO2.

    Techniques: Genome Wide, Labeling

    FCGR2B expression correlates with poor prognosis and aggressive phenotypes in HGSOC. (A) Expression of FCGR2B in TCGA ovarian tumors (TCGA-OV, n = 426) versus normal ovarian tissues from GTEx (n = 88), shown as log2(TPM + 1). (B) Kaplan–Meier curves for PFS in GEO-derived HGSOC cohorts (n = 102), stratified by median expression. (C) Validation of PFS in a meta-cohort of 1435 OC samples. (D–F) Clinical associations of FCGR2B expression with tumor grade (D), lymph node invasion (E), and venous invasion (F) using the BEST database. (G) GSEA identifies the five pathways that are significantly enriched in samples with high FCGR2B expression.

    Journal: Translational Oncology

    Article Title: Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining

    doi: 10.1016/j.tranon.2026.102748

    Figure Lengend Snippet: FCGR2B expression correlates with poor prognosis and aggressive phenotypes in HGSOC. (A) Expression of FCGR2B in TCGA ovarian tumors (TCGA-OV, n = 426) versus normal ovarian tissues from GTEx (n = 88), shown as log2(TPM + 1). (B) Kaplan–Meier curves for PFS in GEO-derived HGSOC cohorts (n = 102), stratified by median expression. (C) Validation of PFS in a meta-cohort of 1435 OC samples. (D–F) Clinical associations of FCGR2B expression with tumor grade (D), lymph node invasion (E), and venous invasion (F) using the BEST database. (G) GSEA identifies the five pathways that are significantly enriched in samples with high FCGR2B expression.

    Article Snippet: The HGSOC cell lines SK-OV-3 (ATCC® HTB-77TM) and OVCAR-3 (ATCC® HTB-161TM), as well as the human monocytic cell line THP-1 (ATCC® TIB-202TM), were obtained from the American Type Culture Collection and cultured under standard conditions at 37 °C with 5% CO2.

    Techniques: Expressing, Derivative Assay, Biomarker Discovery

    FCGR2B expression defines an immunosuppressive TME in HGSOC. (A) ssGSEA-based immune infiltration analysis across 28 immune cell types. Δ = High - Low. (B) CIBERSORT-based macrophage-focused immune deconvolution reveals distinct immune landscapes between FCGR2B -High and FCGR2B -Low tumors. (C) Fluorescence images (scale bar, 50 μm) of FCGR2B (red), CD14 (green), CD68 (yellow), and the corresponding merged image. (D-E) Quantitative analysis of FCGR2B co-localization with CD14 (D) and CD68 (E). Left: box plots comparing co-localization levels between FCGR2B-High and FCGR2B-Low tumors (defined by the median FCGR2B H-score; Wilcoxon rank-sum test). Right: scatter plots showing correlations between FCGR2B and marker H-scores across all HGSOC samples (Spearman’s rho). (F) FCGR2B protein expression in HGSOC cell lines (SKOV3 and OVCAR3) and the cell line THP-1, as detected by WB assays. (G) FCGR2B protein expression in THP-1 cells transfected with Si-FCGR2B or control siRNA, as detected by WB assays. (H) Effect of FCGR2B knockdown on macrophage M2 polarization (CD206⁺/CD68⁺) under SKOV3 (HGSOC) co-culture conditions, assessed by flow cytometry. (I) Effect of FCGR2B knockdown on macrophage phagocytosis (CD68⁺/CFSE⁺) of SKOV3 cells under co-culture conditions, analyzed by flow cytometry. Statistical significance was determined using a two-tailed unpaired Student’s t -test; exact P values are indicated within the figure ( P = 0.0001, t = 14.35 for H; P = 0.0013, t = 7.976 for I; n =3, df = 4).

    Journal: Translational Oncology

    Article Title: Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining

    doi: 10.1016/j.tranon.2026.102748

    Figure Lengend Snippet: FCGR2B expression defines an immunosuppressive TME in HGSOC. (A) ssGSEA-based immune infiltration analysis across 28 immune cell types. Δ = High - Low. (B) CIBERSORT-based macrophage-focused immune deconvolution reveals distinct immune landscapes between FCGR2B -High and FCGR2B -Low tumors. (C) Fluorescence images (scale bar, 50 μm) of FCGR2B (red), CD14 (green), CD68 (yellow), and the corresponding merged image. (D-E) Quantitative analysis of FCGR2B co-localization with CD14 (D) and CD68 (E). Left: box plots comparing co-localization levels between FCGR2B-High and FCGR2B-Low tumors (defined by the median FCGR2B H-score; Wilcoxon rank-sum test). Right: scatter plots showing correlations between FCGR2B and marker H-scores across all HGSOC samples (Spearman’s rho). (F) FCGR2B protein expression in HGSOC cell lines (SKOV3 and OVCAR3) and the cell line THP-1, as detected by WB assays. (G) FCGR2B protein expression in THP-1 cells transfected with Si-FCGR2B or control siRNA, as detected by WB assays. (H) Effect of FCGR2B knockdown on macrophage M2 polarization (CD206⁺/CD68⁺) under SKOV3 (HGSOC) co-culture conditions, assessed by flow cytometry. (I) Effect of FCGR2B knockdown on macrophage phagocytosis (CD68⁺/CFSE⁺) of SKOV3 cells under co-culture conditions, analyzed by flow cytometry. Statistical significance was determined using a two-tailed unpaired Student’s t -test; exact P values are indicated within the figure ( P = 0.0001, t = 14.35 for H; P = 0.0013, t = 7.976 for I; n =3, df = 4).

    Article Snippet: The HGSOC cell lines SK-OV-3 (ATCC® HTB-77TM) and OVCAR-3 (ATCC® HTB-161TM), as well as the human monocytic cell line THP-1 (ATCC® TIB-202TM), were obtained from the American Type Culture Collection and cultured under standard conditions at 37 °C with 5% CO2.

    Techniques: Expressing, Fluorescence, Marker, Transfection, Control, Knockdown, Co-Culture Assay, Flow Cytometry, Two Tailed Test

    FCGR2B-mediated transcriptomic alterations and its impact on HGSOC cell survival. (A) Myeloid-lineage-specific drug sensitivity analysis across DepMap cell lines. The volcano plot shows compounds whose sensitivity (AUC) significantly correlates with FCGR2B expression ( P < 0.05, r < -0.3). The top negatively correlated drug is labeled. (B) Correlation between FCGR2B mRNA expression (log 2 [TPM + 1]) and sensitivity (AUC) to the ARRY-886 (GDSC1:1062) across 24 myeloid-derived cell lines. (C) Volcano plot showing differentially expressed genes in FCGR2B-knockdown versus control macrophages. Upregulated and downregulated genes are highlighted. (D) KEGG pathway enrichment analysis of differentially expressed genes. (E) GSEA of the TNF-α signaling via NF-κB hallmark pathway in FCGR2B-knockdown versus control macrophages. (F) Proliferation assay of SKOV3 cells treated with CM derived from Si-NC or Si-FCGR2B transfected macrophages, assessed by CCK-8 assay. (G) Flow cytometric analysis and quantification of SKOV3 cell apoptosis following treatment with the indicated macrophage CM. *** P < 0.001, **** P < 0.0001 by ANOVA (F) or Student's t -test (G).

    Journal: Translational Oncology

    Article Title: Unmasking FCGR2B as a high-grade serous ovarian cancer specific marker of immune suppression and tumor progression through multi-omics mining

    doi: 10.1016/j.tranon.2026.102748

    Figure Lengend Snippet: FCGR2B-mediated transcriptomic alterations and its impact on HGSOC cell survival. (A) Myeloid-lineage-specific drug sensitivity analysis across DepMap cell lines. The volcano plot shows compounds whose sensitivity (AUC) significantly correlates with FCGR2B expression ( P < 0.05, r < -0.3). The top negatively correlated drug is labeled. (B) Correlation between FCGR2B mRNA expression (log 2 [TPM + 1]) and sensitivity (AUC) to the ARRY-886 (GDSC1:1062) across 24 myeloid-derived cell lines. (C) Volcano plot showing differentially expressed genes in FCGR2B-knockdown versus control macrophages. Upregulated and downregulated genes are highlighted. (D) KEGG pathway enrichment analysis of differentially expressed genes. (E) GSEA of the TNF-α signaling via NF-κB hallmark pathway in FCGR2B-knockdown versus control macrophages. (F) Proliferation assay of SKOV3 cells treated with CM derived from Si-NC or Si-FCGR2B transfected macrophages, assessed by CCK-8 assay. (G) Flow cytometric analysis and quantification of SKOV3 cell apoptosis following treatment with the indicated macrophage CM. *** P < 0.001, **** P < 0.0001 by ANOVA (F) or Student's t -test (G).

    Article Snippet: The HGSOC cell lines SK-OV-3 (ATCC® HTB-77TM) and OVCAR-3 (ATCC® HTB-161TM), as well as the human monocytic cell line THP-1 (ATCC® TIB-202TM), were obtained from the American Type Culture Collection and cultured under standard conditions at 37 °C with 5% CO2.

    Techniques: Expressing, Labeling, Derivative Assay, Knockdown, Control, Proliferation Assay, Transfection, CCK-8 Assay

    (A) Schematic representation of hsa-miR-15a and MTX-5-FU-Gem-miR-15a, showing incorporation of 5-fluorouracil and gemcitabine into the miR-15a backbone and conjugation of methotrexate (MTX) to the passenger strand. (B-E) Dose-response curves showing cell viability following treatment with MTX-5-FU-Gem-miR-15a, unmodified miR-15a, and olaparib in SK-OV-3 (B), OVCAR-3 (C), A2780 (D), and UWB1.289 (E) cells. Data represent mean ± SD from n = 4 biological replicates.

    Journal: bioRxiv

    Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

    doi: 10.64898/2026.04.20.719456

    Figure Lengend Snippet: (A) Schematic representation of hsa-miR-15a and MTX-5-FU-Gem-miR-15a, showing incorporation of 5-fluorouracil and gemcitabine into the miR-15a backbone and conjugation of methotrexate (MTX) to the passenger strand. (B-E) Dose-response curves showing cell viability following treatment with MTX-5-FU-Gem-miR-15a, unmodified miR-15a, and olaparib in SK-OV-3 (B), OVCAR-3 (C), A2780 (D), and UWB1.289 (E) cells. Data represent mean ± SD from n = 4 biological replicates.

    Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

    Techniques: Conjugation Assay

    (A) Representative histograms of DNA content (PI staining) in only negative control and MTX-5-FU-Gem-miR-15a treatment showing cell cycle distribution in SK-OV-3, OVCAR-3, A2780, and UWB1.289 cells following treatment. (B) Quantification of cell cycle distribution after treatment shown as fold change in G2/S ratio relative to negative control across cell lines. (C) Representative Annexin V/PI flow cytometry plots showing apoptosis in indicated cell lines. (D) Quantification of apoptotic cells (early + late apoptosis) shown as fold change relative to control. (E) Western blot analysis showing expression of cleaved PARP, BCL-2, BAX, and BAK following treatment; β-actin serves as a loading control. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

    doi: 10.64898/2026.04.20.719456

    Figure Lengend Snippet: (A) Representative histograms of DNA content (PI staining) in only negative control and MTX-5-FU-Gem-miR-15a treatment showing cell cycle distribution in SK-OV-3, OVCAR-3, A2780, and UWB1.289 cells following treatment. (B) Quantification of cell cycle distribution after treatment shown as fold change in G2/S ratio relative to negative control across cell lines. (C) Representative Annexin V/PI flow cytometry plots showing apoptosis in indicated cell lines. (D) Quantification of apoptotic cells (early + late apoptosis) shown as fold change relative to control. (E) Western blot analysis showing expression of cleaved PARP, BCL-2, BAX, and BAK following treatment; β-actin serves as a loading control. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

    Techniques: Staining, Negative Control, Flow Cytometry, Control, Western Blot, Expressing, Two Tailed Test

    (A, C, E) Western blot analysis of canonical miR-15a target proteins in ovarian cancer cells treated with negative control, miR-15a, MTX-5-FU-Gem-miR-15a, or 5-FU + gemcitabine. Panel A, SK-OV-3; panel C, OVCAR-3; panel E, UWB1.289. (B, D, F) Densitometric quantification of the corresponding western blots normalized to β-actin. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

    doi: 10.64898/2026.04.20.719456

    Figure Lengend Snippet: (A, C, E) Western blot analysis of canonical miR-15a target proteins in ovarian cancer cells treated with negative control, miR-15a, MTX-5-FU-Gem-miR-15a, or 5-FU + gemcitabine. Panel A, SK-OV-3; panel C, OVCAR-3; panel E, UWB1.289. (B, D, F) Densitometric quantification of the corresponding western blots normalized to β-actin. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

    Techniques: Western Blot, Negative Control, Two Tailed Test

    (A-C) Dose-response curves for MTX-5-FU-Gem-miR-15a and olaparib in olaparib-resistant OVCAR-3/OlaR (A), SK-OV-3/OlaR (B), and UWB1.289/OlaR (C) cells. (D) Representative cell cycle histograms (PI staining) and quantification of fold change in G2/S ratio in resistant cell lines. (E) Representative Annexin V/PI plots and quantification of total apoptotic cells (early + late apoptosis). (F-G) Dose-response analysis of cell viability in OVCAR-3 (F) and SK-OV-3 (G) spheroid cultures treated with increasing concentrations of MTX-5-FU-Gem-miR-15a or olaparib. (H) Western blot analysis of WEE1, CHK1, CCND1, and BCL-2 in OVCAR-3 spheroid cultures following treatment; β-actin serves as the loading control. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

    doi: 10.64898/2026.04.20.719456

    Figure Lengend Snippet: (A-C) Dose-response curves for MTX-5-FU-Gem-miR-15a and olaparib in olaparib-resistant OVCAR-3/OlaR (A), SK-OV-3/OlaR (B), and UWB1.289/OlaR (C) cells. (D) Representative cell cycle histograms (PI staining) and quantification of fold change in G2/S ratio in resistant cell lines. (E) Representative Annexin V/PI plots and quantification of total apoptotic cells (early + late apoptosis). (F-G) Dose-response analysis of cell viability in OVCAR-3 (F) and SK-OV-3 (G) spheroid cultures treated with increasing concentrations of MTX-5-FU-Gem-miR-15a or olaparib. (H) Western blot analysis of WEE1, CHK1, CCND1, and BCL-2 in OVCAR-3 spheroid cultures following treatment; β-actin serves as the loading control. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

    Techniques: Staining, Western Blot, Control, Two Tailed Test

    (A) Schematic of the in vivo experimental design and treatment schedule. (B) Representative bioluminescence images of parental SK-OV-3 xenografts at endpoint. (C) Tumor growth curves over time for vehicle- and MTX-5-FU-Gem-miR-15a-treated parental xenografts. (D) Kaplan-Meier survival analysis of parental xenografts. (E) Serum AST and ALT measurements evaluating treatment-associated toxicity. (F) Representative bioluminescence images of resistant SK-OV-3/OlaR xenografts treated with vehicle, intravenous MTX-5-FU-Gem-miR-15a, or intraperitoneal MTX-5-FU-Gem-miR-15a. (G) Tumor growth curves over time for resistant xenografts. (H) Proposed mechanistic model of MTX-5-FU-Gem-miR-15a activity. Data represent mean ± SD. Statistical significance for tumor growth and body weight analyses was determined using two-way ANOVA with appropriate post hoc testing. Survival differences were analyzed using the log-rank (Mantel-Cox) test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

    doi: 10.64898/2026.04.20.719456

    Figure Lengend Snippet: (A) Schematic of the in vivo experimental design and treatment schedule. (B) Representative bioluminescence images of parental SK-OV-3 xenografts at endpoint. (C) Tumor growth curves over time for vehicle- and MTX-5-FU-Gem-miR-15a-treated parental xenografts. (D) Kaplan-Meier survival analysis of parental xenografts. (E) Serum AST and ALT measurements evaluating treatment-associated toxicity. (F) Representative bioluminescence images of resistant SK-OV-3/OlaR xenografts treated with vehicle, intravenous MTX-5-FU-Gem-miR-15a, or intraperitoneal MTX-5-FU-Gem-miR-15a. (G) Tumor growth curves over time for resistant xenografts. (H) Proposed mechanistic model of MTX-5-FU-Gem-miR-15a activity. Data represent mean ± SD. Statistical significance for tumor growth and body weight analyses was determined using two-way ANOVA with appropriate post hoc testing. Survival differences were analyzed using the log-rank (Mantel-Cox) test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

    Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

    Techniques: In Vivo, Activity Assay

    Higher expression of CDK9 was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.

    Journal: Scientific Reports

    Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

    doi: 10.1038/s41598-026-47843-6

    Figure Lengend Snippet: Higher expression of CDK9 was present in the resistant ovarian cancer cell line compared to the parental sensitive cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of paclitaxel for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of paclitaxel for five days. ( C ) Expression levels of CDK9 and related signaling pathway proteins involved in transcription in SKOV3TR and OVCAR8TR, and parental sensitive cell lines SKOV3 and OVCAR8 were determined by Western blot. There are 2 isoforms of the CDK9 protein: the 42 kDa CDK9 isoform and the 55 kDa isoform. The smaller 42 kDa isoform was the first identified isoform. The larger, 55 kDa isoform has a characteristic 117 residue terminal expansion. ( D ) Relative expression of both CDK9 isoforms and α-Tubulin in the ovarian cancer cell lines. ** P < 0.01.

    Article Snippet: The human ovarian cancer cell line SKOV3 was purchased from the American Type Culture Collection (Rockville, MD) in 2014 with certificate of analysis.

    Techniques: Expressing, Incubation, Concentration Assay, Western Blot, Residue

    Effects of combination treatment with paclitaxel and CDK9 inhibitor LDC067 on the viability of multidrug resistant ovarian cancer cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( C and D ) Relative cell viability of SKOV3TR and OVCAR8TR cells in combination with paclitaxel and CDK9 inhibitor LDC067 for five days. N.S. indicates that the observed data for paclitaxel and LDC067 alone treated groups are not statistically significant as compared with untreated groups; * P < 0.05, the observed data for paclitaxel and LDC067 combinatorial treated groups are statistically significant as compared with the untreated groups; ** P < 0.01, the observed results for paclitaxel and LDC067 combinatorial treated groups are highly statistically significant as compared with the untreated groups.

    Journal: Scientific Reports

    Article Title: Inhibition of CDK9 sensitizes multidrug resistant ovarian cancer cells to paclitaxel

    doi: 10.1038/s41598-026-47843-6

    Figure Lengend Snippet: Effects of combination treatment with paclitaxel and CDK9 inhibitor LDC067 on the viability of multidrug resistant ovarian cancer cell line. ( A ) Relative cell viability of SKOV3 and SKOV3TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( B ) Relative cell viability of OVCAR8 and OVCAR8TR cells after incubation with different concentration of CDK9 inhibitor LDC067 for five days. ( C and D ) Relative cell viability of SKOV3TR and OVCAR8TR cells in combination with paclitaxel and CDK9 inhibitor LDC067 for five days. N.S. indicates that the observed data for paclitaxel and LDC067 alone treated groups are not statistically significant as compared with untreated groups; * P < 0.05, the observed data for paclitaxel and LDC067 combinatorial treated groups are statistically significant as compared with the untreated groups; ** P < 0.01, the observed results for paclitaxel and LDC067 combinatorial treated groups are highly statistically significant as compared with the untreated groups.

    Article Snippet: The human ovarian cancer cell line SKOV3 was purchased from the American Type Culture Collection (Rockville, MD) in 2014 with certificate of analysis.

    Techniques: Incubation, Concentration Assay