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human ovarian cancer cell lines ov90  (ATCC)


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    ATCC human ovarian cancer cell lines ov90
    A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and <t>OV90</t> cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Human Ovarian Cancer Cell Lines Ov90, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 407 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human ovarian cancer cell lines ov90/product/ATCC
    Average 96 stars, based on 407 article reviews
    human ovarian cancer cell lines ov90 - by Bioz Stars, 2026-05
    96/100 stars

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    1) Product Images from "Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function"

    Article Title: Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-026-08495-6

    A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and OV90 cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Figure Legend Snippet: A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and OV90 cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Techniques Used: Derivative Assay, Expressing, Transfection, Negative Control, Alternative Splicing, Binding Assay, RNA Sequencing, Quantitative RT-PCR, Knockdown, Positive Control, Pull Down Assay, Western Blot, Over Expression, Control



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    human ovarian cancer cell lines ov90  (ATCC)
    96
    ATCC human ovarian cancer cell lines ov90
    A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and <t>OV90</t> cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Human Ovarian Cancer Cell Lines 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
    https://www.bioz.com/result/human ovarian cancer cell lines ov90/product/ATCC
    Average 96 stars, based on 1 article reviews
    human ovarian cancer cell lines ov90 - by Bioz Stars, 2026-05
    96/100 stars
    		  Buy from Supplier
    human ovarian cancer cell line ov90  (ATCC)
    96
    ATCC human ovarian cancer cell line ov90
    OV effectively delivers BCMAt to solid tumors and redirects activation and cytotoxicity of BCMA-CAR T cells and human T cells in the presence of BCMA-TCE in vitro. ( a ) Illustration of vaccinia OV with BCMAt incorporated under the control of the synthetic early promoter inserted into the J2R locus and replacing the tk gene (OVBCMAt). ( b ) Quantification of BCMAt expression on various solid tumor cell lines 24 (left) and 48 hours (right) after exposure to indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated two times. ( c–e ) Quantification of CD137 expression (left), tumor cell killing (middle), and BCMAt expression (right) assessed by flow cytometry after 24 hours of ( c ) MDA-MB-468, ( d ) SNU-16, or ( e ) <t>OV90</t> tumor cells co-cultured with or without BCMA-TCE in the presence of human T cells or BCMA-CAR T cells and indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated three times. P values indicate differences between BCMA-TCE groups with PBMCs and PBMCs only determined using unpaired Student’s t-test (*p<0.05, **p<0.01, and ***p<0.005; ns=not significant). BCMAt, truncated B cell maturation antigen; CAR, chimeric antigen receptor; MOI, multiplicity of infection; OV, oncolytic virus, OVBCMAt, OV carrying the BCMAt-encoding gene; PBMC, peripheral blood mononuclear cell; TCE, T cell engager; tk, thymidine kinase; UTD, untransduced.
    Human 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
    https://www.bioz.com/result/human ovarian cancer cell line ov90/product/ATCC
    Average 96 stars, based on 1 article reviews
    human ovarian cancer cell line ov90 - by Bioz Stars, 2026-05
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    ov90 ovarian cancer cell line atcc crl 11732 human  (ATCC)
    96
    ATCC ov90 ovarian cancer cell line atcc crl 11732 human
    OV effectively delivers BCMAt to solid tumors and redirects activation and cytotoxicity of BCMA-CAR T cells and human T cells in the presence of BCMA-TCE in vitro. ( a ) Illustration of vaccinia OV with BCMAt incorporated under the control of the synthetic early promoter inserted into the J2R locus and replacing the tk gene (OVBCMAt). ( b ) Quantification of BCMAt expression on various solid tumor cell lines 24 (left) and 48 hours (right) after exposure to indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated two times. ( c–e ) Quantification of CD137 expression (left), tumor cell killing (middle), and BCMAt expression (right) assessed by flow cytometry after 24 hours of ( c ) MDA-MB-468, ( d ) SNU-16, or ( e ) <t>OV90</t> tumor cells co-cultured with or without BCMA-TCE in the presence of human T cells or BCMA-CAR T cells and indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated three times. P values indicate differences between BCMA-TCE groups with PBMCs and PBMCs only determined using unpaired Student’s t-test (*p<0.05, **p<0.01, and ***p<0.005; ns=not significant). BCMAt, truncated B cell maturation antigen; CAR, chimeric antigen receptor; MOI, multiplicity of infection; OV, oncolytic virus, OVBCMAt, OV carrying the BCMAt-encoding gene; PBMC, peripheral blood mononuclear cell; TCE, T cell engager; tk, thymidine kinase; UTD, untransduced.
    Ov90 Ovarian Cancer Cell Line Atcc Crl 11732 Human, 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
    https://www.bioz.com/result/ov90 ovarian cancer cell line atcc crl 11732 human/product/ATCC
    Average 96 stars, based on 1 article reviews
    ov90 ovarian cancer cell line atcc crl 11732 human - by Bioz Stars, 2026-05
    96/100 stars
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    ov90 human serous ovarian cancer cell lines  (ATCC)
    96
    ATCC ov90 human serous ovarian cancer cell lines
    Carboplatin-resistant ovarian cancer exhibited rewired oxidize redox state “high level ROS while low level antioxidants”. (a) Intracellular peroxides levels measured by DCF fluorescence probe. PEG-CAT (500 units) were added 24 hr prior to the assay. (b) Extracellular H 2 O 2 levels in the media after 24-hr culturing. Amplex Red was used for the assay. (c) Intracellular of H 2 O 2 in picomole after 24-h culturing. (d) Western blot assay for the steady-state level of antioxidant proteins. Lysates were collected after 24-hr culturing. (e) Antioxidant activities. Cells were collected after 24-hr culturing and sonicated for lysates. MnSOD activity was measured using activity gel with NBT. GPx activity was assessed using a commercial kit. Oxidized form of Trx1 was measured with redox western blot assay. ∗ P ≤ .05 versus hTER7 group. # P ≤ .05 versus <t>OV90</t> group.
    Ov90 Human Serous Ovarian Cancer Cell Lines, 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
    https://www.bioz.com/result/ov90 human serous ovarian cancer cell lines/product/ATCC
    Average 96 stars, based on 1 article reviews
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    A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and OV90 cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Cell Death & Disease

    Article Title: Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function

    doi: 10.1038/s41419-026-08495-6

    Figure Lengend Snippet: A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and OV90 cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Human ovarian cancer cell lines OV90, SKOV3, OVCAR3, OVCAR8, and CAOV3 were purchased from the American Type Culture Collection.

    Techniques: Derivative Assay, Expressing, Transfection, Negative Control, Alternative Splicing, Binding Assay, RNA Sequencing, Quantitative RT-PCR, Knockdown, Positive Control, Pull Down Assay, Western Blot, Over Expression, Control

    OV effectively delivers BCMAt to solid tumors and redirects activation and cytotoxicity of BCMA-CAR T cells and human T cells in the presence of BCMA-TCE in vitro. ( a ) Illustration of vaccinia OV with BCMAt incorporated under the control of the synthetic early promoter inserted into the J2R locus and replacing the tk gene (OVBCMAt). ( b ) Quantification of BCMAt expression on various solid tumor cell lines 24 (left) and 48 hours (right) after exposure to indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated two times. ( c–e ) Quantification of CD137 expression (left), tumor cell killing (middle), and BCMAt expression (right) assessed by flow cytometry after 24 hours of ( c ) MDA-MB-468, ( d ) SNU-16, or ( e ) OV90 tumor cells co-cultured with or without BCMA-TCE in the presence of human T cells or BCMA-CAR T cells and indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated three times. P values indicate differences between BCMA-TCE groups with PBMCs and PBMCs only determined using unpaired Student’s t-test (*p<0.05, **p<0.01, and ***p<0.005; ns=not significant). BCMAt, truncated B cell maturation antigen; CAR, chimeric antigen receptor; MOI, multiplicity of infection; OV, oncolytic virus, OVBCMAt, OV carrying the BCMAt-encoding gene; PBMC, peripheral blood mononuclear cell; TCE, T cell engager; tk, thymidine kinase; UTD, untransduced.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Universal off-the-shelf combination immunotherapy using oncolytic viruses to redirect T cell engagers to target solid tumors

    doi: 10.1136/jitc-2024-011051

    Figure Lengend Snippet: OV effectively delivers BCMAt to solid tumors and redirects activation and cytotoxicity of BCMA-CAR T cells and human T cells in the presence of BCMA-TCE in vitro. ( a ) Illustration of vaccinia OV with BCMAt incorporated under the control of the synthetic early promoter inserted into the J2R locus and replacing the tk gene (OVBCMAt). ( b ) Quantification of BCMAt expression on various solid tumor cell lines 24 (left) and 48 hours (right) after exposure to indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated two times. ( c–e ) Quantification of CD137 expression (left), tumor cell killing (middle), and BCMAt expression (right) assessed by flow cytometry after 24 hours of ( c ) MDA-MB-468, ( d ) SNU-16, or ( e ) OV90 tumor cells co-cultured with or without BCMA-TCE in the presence of human T cells or BCMA-CAR T cells and indicated MOI of OVBCMAt. n=2 per condition and each experiment was repeated three times. P values indicate differences between BCMA-TCE groups with PBMCs and PBMCs only determined using unpaired Student’s t-test (*p<0.05, **p<0.01, and ***p<0.005; ns=not significant). BCMAt, truncated B cell maturation antigen; CAR, chimeric antigen receptor; MOI, multiplicity of infection; OV, oncolytic virus, OVBCMAt, OV carrying the BCMAt-encoding gene; PBMC, peripheral blood mononuclear cell; TCE, T cell engager; tk, thymidine kinase; UTD, untransduced.

    Article Snippet: Human ovarian cancer cell line OV90 (ATCC CRL-11732) was cultured in 1:1 vol of MCDB 105 medium (Sigma-Aldrich) and medium 199 (Gibco) containing 20% FBS and 1× AA.

    Techniques: Activation Assay, In Vitro, Control, Expressing, Flow Cytometry, Cell Culture, Infection, Virus

    Carboplatin-resistant ovarian cancer exhibited rewired oxidize redox state “high level ROS while low level antioxidants”. (a) Intracellular peroxides levels measured by DCF fluorescence probe. PEG-CAT (500 units) were added 24 hr prior to the assay. (b) Extracellular H 2 O 2 levels in the media after 24-hr culturing. Amplex Red was used for the assay. (c) Intracellular of H 2 O 2 in picomole after 24-h culturing. (d) Western blot assay for the steady-state level of antioxidant proteins. Lysates were collected after 24-hr culturing. (e) Antioxidant activities. Cells were collected after 24-hr culturing and sonicated for lysates. MnSOD activity was measured using activity gel with NBT. GPx activity was assessed using a commercial kit. Oxidized form of Trx1 was measured with redox western blot assay. ∗ P ≤ .05 versus hTER7 group. # P ≤ .05 versus OV90 group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: Carboplatin-resistant ovarian cancer exhibited rewired oxidize redox state “high level ROS while low level antioxidants”. (a) Intracellular peroxides levels measured by DCF fluorescence probe. PEG-CAT (500 units) were added 24 hr prior to the assay. (b) Extracellular H 2 O 2 levels in the media after 24-hr culturing. Amplex Red was used for the assay. (c) Intracellular of H 2 O 2 in picomole after 24-h culturing. (d) Western blot assay for the steady-state level of antioxidant proteins. Lysates were collected after 24-hr culturing. (e) Antioxidant activities. Cells were collected after 24-hr culturing and sonicated for lysates. MnSOD activity was measured using activity gel with NBT. GPx activity was assessed using a commercial kit. Oxidized form of Trx1 was measured with redox western blot assay. ∗ P ≤ .05 versus hTER7 group. # P ≤ .05 versus OV90 group.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Fluorescence, Western Blot, Sonication, Activity Assay

    Increased mitochondrial respiratory and glycolytic activity are linked with carboplatin-resistant cancer. (a) Parameters of mitochondrial function calculated from OCR. (b) Glycolytic activity calculated from ECAR of live OV90 cells and OVCD cells. # P ≤ .05 versus OV90 group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: Increased mitochondrial respiratory and glycolytic activity are linked with carboplatin-resistant cancer. (a) Parameters of mitochondrial function calculated from OCR. (b) Glycolytic activity calculated from ECAR of live OV90 cells and OVCD cells. # P ≤ .05 versus OV90 group.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Activity Assay

    MnP sensitized resistant ovarian cancer to carboplatin while protecting normal cells from chemotherapy-induced injury. Cells were cultured for 24 prior to treatment with 50 nM MnP and/or CBCD (7 μ M). (a) OV90 cell viability and (b) OVCD cell viability after treatment of MnP and/or CBCD (24 hr). (c) hTER7 cell viability after treatment of MnP and/or CBCD, CDDP, PTX (24 hr). % Cell viability was normalized to no-treatment. ∗ P ≤ .05 versus hTER7 group. ∗∗ P ≤ .05 versus CBDCA alone.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: MnP sensitized resistant ovarian cancer to carboplatin while protecting normal cells from chemotherapy-induced injury. Cells were cultured for 24 prior to treatment with 50 nM MnP and/or CBCD (7 μ M). (a) OV90 cell viability and (b) OVCD cell viability after treatment of MnP and/or CBCD (24 hr). (c) hTER7 cell viability after treatment of MnP and/or CBCD, CDDP, PTX (24 hr). % Cell viability was normalized to no-treatment. ∗ P ≤ .05 versus hTER7 group. ∗∗ P ≤ .05 versus CBDCA alone.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Cell Culture

    MnP and carboplatin concentration analysis using LC/MS after 1-hr treatment.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: MnP and carboplatin concentration analysis using LC/MS after 1-hr treatment.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Concentration Assay

    Increasing oxidative stress in cancer by cotreatment of MnP and carboplatin. (a) Intracellular peroxide levels measured by DCF fluorescence probe after 2-hr treatment. PEG-CAT (500 units) were added 24 hr prior to the assay. (b) Intracellular H 2 O 2 levels after 2-hr treatment. (c) Catalase activity after 2-hr treatment. (d) GSH levels were measured by HPLC after 24-hr treatment. (e) MnSOD activity was measured using activity gel with NBT, after 24-hr treatment. (f) GPx activity was determined using a commercial kit after 24-hr treatment. ∗ P ≤ .05 versus hTER7 group. ∗ P ≤ .05 versus no treatment group. # P ≤ .05 versus OV90 group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: Increasing oxidative stress in cancer by cotreatment of MnP and carboplatin. (a) Intracellular peroxide levels measured by DCF fluorescence probe after 2-hr treatment. PEG-CAT (500 units) were added 24 hr prior to the assay. (b) Intracellular H 2 O 2 levels after 2-hr treatment. (c) Catalase activity after 2-hr treatment. (d) GSH levels were measured by HPLC after 24-hr treatment. (e) MnSOD activity was measured using activity gel with NBT, after 24-hr treatment. (f) GPx activity was determined using a commercial kit after 24-hr treatment. ∗ P ≤ .05 versus hTER7 group. ∗ P ≤ .05 versus no treatment group. # P ≤ .05 versus OV90 group.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Fluorescence, Activity Assay

    Cotreatment of MnP and carboplatin inhibited mitochondrial respiratory and ATP production in chemoresistant ovarian cancer cells. MnP and/or CBDCA were added to the cells for 6 hr. Live cells were then used for the measurement of OCR and ECAR in OV90 cells (a and c) and in OVCD cells (b and d). (e) Absolute ATP concentration was measured using ATP kits after 24-hr treatment. ∗ P ≤ .05 versus control.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: Cotreatment of MnP and carboplatin inhibited mitochondrial respiratory and ATP production in chemoresistant ovarian cancer cells. MnP and/or CBDCA were added to the cells for 6 hr. Live cells were then used for the measurement of OCR and ECAR in OV90 cells (a and c) and in OVCD cells (b and d). (e) Absolute ATP concentration was measured using ATP kits after 24-hr treatment. ∗ P ≤ .05 versus control.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Concentration Assay, Control

    MnP-mediated oxidative stress inhibited Nrf2 and its downstream target, Trx1 in ovarian cancer carboplatin-resistant cell but not in a normal cell. Cells were cultured for 24 hr prior to MnP treatment (6 hr). Cells were then collected, and RNA was isolated for RT-PCR. (a) Nrf2 and its downstream targets were compared between hTER7, OV90, and OVCD cells. Nrf2 and its downstream targets in (b) hTER7 cell line, (c) OV90 cell line, and (d) OVCD cell line, after MnP treatment. (e) Immunoprecipitation (IP) is performed with antibody to Trx1 and western blot analysis with anti-Keap1, Nrf2, and Trx1 antibodies were subsequently performed. ∗ P ≤ .05 when compared to control.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP 5+ , Synergizes with Carboplatin in Treatment of Chemoresistant Ovarian Cell Line

    doi: 10.1155/2022/9664636

    Figure Lengend Snippet: MnP-mediated oxidative stress inhibited Nrf2 and its downstream target, Trx1 in ovarian cancer carboplatin-resistant cell but not in a normal cell. Cells were cultured for 24 hr prior to MnP treatment (6 hr). Cells were then collected, and RNA was isolated for RT-PCR. (a) Nrf2 and its downstream targets were compared between hTER7, OV90, and OVCD cells. Nrf2 and its downstream targets in (b) hTER7 cell line, (c) OV90 cell line, and (d) OVCD cell line, after MnP treatment. (e) Immunoprecipitation (IP) is performed with antibody to Trx1 and western blot analysis with anti-Keap1, Nrf2, and Trx1 antibodies were subsequently performed. ∗ P ≤ .05 when compared to control.

    Article Snippet: OV90 human serous ovarian cancer cell lines were purchased from ATCC.

    Techniques: Cell Culture, Isolation, Reverse Transcription Polymerase Chain Reaction, Immunoprecipitation, Western Blot, Control