We are analyzing https://link.springer.com/article/10.1186/s12935-020-01500-8.

Title:
XIST lost induces ovarian cancer stem cells to acquire taxol resistance via a KMT2C-dependent way | Cancer Cell International
Description:
Background/aims The expression levels of long non-coding RNA XIST are significantly associated with paclitaxel (Pac) sensitivity in ovarian cancer, but the mechanism of action remains unclear. Therefore, this experimental design was based on lncRNA XIST analysis to regulate the effect of XIST on the tumor stem cell and paclitaxel sensitivity in ovarian cancer. Methods Sphere assay and fluorescence activated cell sorting (FACS) were used to determine the expression levels of XIST and sensitivity to paclitaxel treatment. The effect of the proliferation was detected by MTT assay. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for lncRNA XIS and KMT2C. The expression of KMT2C was detected by RT-qPCR and Western blotting. RT-qPCR was used to detect the expression of cancer stem cell-associated genes SOX2, OCT4 and Nanog. The tumor changes in mice were detected by in vivo experiments in nude mice. Results There was an inverse correlation between the expression of XIST and cancer stem cell (CD44 + /CD24−) population. XIST promoted methylation of histone H3 methylation at lysine 4 by enhancing the stability of lysine (K)-specific methyltransferase 2C (KMT2C) mRNA. XIST acted on the stability of KMT2C mRNA by directly targeting miR-93-5p. Overexpression of miR-93-5p can reverse the XIST overexpression-induced KMT2C decrease and sphere number increase. Overexpression of KMT2C inhibited XIST silencing-induced proliferation of cancer stem cells, and KMT2C was able to mediate paclitaxel resistance induced by XIST in ovarian cancer. The study found that XIST can affect the expression of KMT2C in the ovarian cancer via targeting miR-93-5p. Conclusion XIST promoted the sensitivity of ovarian cancer stem cells to paclitaxel in a KMT2C-dependent manner.
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Keywords {🔍}

xist, cancer, expression, kmtc, cells, ovarian, article, cell, google, scholar, pubmed, stem, skov, fig, overexpression, tovg, cas, levels, significantly, tumor, mirp, lncrna, paclitaxel, sensitivity, resistance, group, mrna, analysis, tumors, assay, patients, tovgoe, rna, tissues, shown, skovkd, central, studies, usa, data, noncoding, treatment, sfe, compared, research, taxol, effect, luciferase, study, regulation,

Topics {✒️}

lncrna xist/mir-200c regulates pe-conjugated cd24 antibody sk-kd + 2c-oe group compared taxol-resistant skov3/txr cell year disease-free survival x-chromosome inactivation center article download pdf t-oe + 2c-kd compared increases multi-drug resistance xist taxol-resistant skov3-kd quantitative real-time pcr targeting mir-130a-3p aging-related viscoelasticity variation 10 ng/ml basic fibroblasts advanced-stage ovarian cancer sk-kd + 2c-oe prospective nation-wide study serum-free medium supplemented cd44 + /cd24−population cells t-oe + 2c-kd wild-type xist reversed tumor-lymph node metastasis directly targeting mir-93-5p year survival rate mirna93-5p overexpression group cancer stem cell cancer stem cell anti-cancer drug resistance tumor stem cell human ovarian cancer cancer stem cells tumor stem cells epithelial ovarian cancer mediate xist-induced skov3-kd+2c oe anti-igg antibody stem cell division specific methyltransferase 2c tov21g-oe+2c kd skov3 cell induced tendon stem cells cancer cell int privacy choices/manage cookies cancer specimens provided xist effectively inhibited tov21g-oe group showed ovarian cancer cells lncrna-mirna interactions tov21g cell induced improving survival rate

Schema {🗺️}

WebPage:
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         headline:XIST lost induces ovarian cancer stem cells to acquire taxol resistance via a KMT2C-dependent way
         description:The expression levels of long non-coding RNA XIST are significantly associated with paclitaxel (Pac) sensitivity in ovarian cancer, but the mechanism of action remains unclear. Therefore, this experimental design was based on lncRNA XIST analysis to regulate the effect of XIST on the tumor stem cell and paclitaxel sensitivity in ovarian cancer. Sphere assay and fluorescence activated cell sorting (FACS) were used to determine the expression levels of XIST and sensitivity to paclitaxel treatment. The effect of the proliferation was detected by MTT assay. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for lncRNA XIS and KMT2C. The expression of KMT2C was detected by RT-qPCR and Western blotting. RT-qPCR was used to detect the expression of cancer stem cell-associated genes SOX2, OCT4 and Nanog. The tumor changes in mice were detected by in vivo experiments in nude mice. There was an inverse correlation between the expression of XIST and cancer stem cell (CD44 + /CD24−) population. XIST promoted methylation of histone H3 methylation at lysine 4 by enhancing the stability of lysine (K)-specific methyltransferase 2C (KMT2C) mRNA. XIST acted on the stability of KMT2C mRNA by directly targeting miR-93-5p. Overexpression of miR-93-5p can reverse the XIST overexpression-induced KMT2C decrease and sphere number increase. Overexpression of KMT2C inhibited XIST silencing-induced proliferation of cancer stem cells, and KMT2C was able to mediate paclitaxel resistance induced by XIST in ovarian cancer. The study found that XIST can affect the expression of KMT2C in the ovarian cancer via targeting miR-93-5p. XIST promoted the sensitivity of ovarian cancer stem cells to paclitaxel in a KMT2C-dependent manner.
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            Cancer Research
            Cell Biology
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      headline:XIST lost induces ovarian cancer stem cells to acquire taxol resistance via a KMT2C-dependent way
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         Ovarian cancer
         Tumor stem cells
         Proliferation
         Cancer Research
         Cell Biology
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