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首页> 外文期刊>Cancer genetics and cytogenetics >Role of STAT3 decoy oligodeoxynucleotides on cell invasion and chemosensitivity in human epithelial ovarian cancer cells.
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Role of STAT3 decoy oligodeoxynucleotides on cell invasion and chemosensitivity in human epithelial ovarian cancer cells.

机译:STAT3诱饵寡聚脱氧核苷酸对人上皮性卵巢癌细胞侵袭和化学敏感性的作用。

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摘要

Recent studies have reported that STAT3 activation is associated with poor prognosis in human epithelial ovarian cancer. STAT3 has been proposed to play an important role in ovarian cancer metastasis and chemoresistance. This mechanism, however, is still not thoroughly understood. In this study, to investigate the role of STAT3 on ovarian cancer cells, we used decoy oligodeoxynucleotide (ODN) technology to regulate STAT3 in SKOV3 and OVCAR3 cells in vitro. Cell invasive power and chemo-sensitivity were assessed in the cells transfected with STAT3 decoy ODN and control ODN. Western blot analysis was used to examine the expression of EMMPRIN, P-gp, and Akt. Results showed that STAT3 decoy ODN inhibited cancer cell invasive power and enhanced sensitivity to paclitaxel for SKOV3 and OVCAR3 cells. The mechanism involved the inhibition of EMMPRIN, P-gp, and pAkt by STAT3 decoy ODN. These three proteins were probably the target proteins of STAT3. These findings suggest that STAT3 is a key factor for ovarian cancer metastasis and chemoresistance. STAT3 decoy ODN may prove to be a beneficial therapeutic agent, especially for invasive or chemoresistant ovarian cancer.
机译:最近的研究报道STAT3激活与人类上皮性卵巢癌预后不良有关。已经提出STAT3在卵巢癌转移和化学抗性中起重要作用。但是,这种机制仍然没有被完全理解。在这项研究中,为了研究STAT3在卵巢癌细胞中的作用,我们使用了诱饵寡聚脱氧核苷酸(ODN)技术在体外调节SKOV3和OVCAR3细胞中的STAT3。在用STAT3诱饵ODN和对照ODN转染的细胞中评估了细胞的侵袭力和化学敏感性。蛋白质印迹分析用于检查EMMPRIN,P-gp和Akt的表达。结果表明,STAT3诱饵ODN抑制癌细胞的侵袭能力,并增强对紫杉醇对SKOV3和OVCAR3细胞的敏感性。该机制涉及STAT3诱饵ODN对EMMPRIN,P-gp和pAkt的抑制。这三种蛋白可能是STAT3的靶蛋白。这些发现表明STAT3是卵巢癌转移和化学抗性的关键因素。 STAT3诱饵ODN可能被证明是有益的治疗剂,尤其是对于浸润性或化学耐药性卵巢癌。

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