Role of STAT3 decoy oligodeoxynucleotides on cell invasion and chemosensitivity in human epithelial ovarian cancer cells
Role of STAT3 decoy oligodeoxynucleotides on cell invasion and chemosensitivity in human epithelial ovarian cancer cells
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STAT3诱饵寡脱氧核苷酸对人上皮性卵巢癌细胞的细胞侵袭和化疗敏感性的作用。
DOI：
10.1016/j.cancergencyto.2009.10.004
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发表时间：
2010-02-01
影响因子：
--
通讯作者：
Yang, Meixiang
中科院分区：
文献类型：
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作者：
Zhang, Xiaolei;Liu, Peishu;Yang, Meixiang
最近的研究报道，STAT3的激活与卵巢上皮癌的预后不良有关。STAT3已被认为在卵巢癌转移和化疗耐药中发挥重要作用。然而，这一机制仍未被彻底理解。为了探讨STAT3在卵巢癌细胞中的作用，本研究利用诱骗寡核苷酸(ODN)技术在体外对SKOV3和OVCAR3细胞中的STAT3进行调控。检测转导STAT3诱骗ODN和对照ODN的细胞侵袭力和化疗敏感性。Western印迹分析检测EMMPRIN、P-gp和Akt的表达。结果表明，STAT3诱骗ODN抑制癌细胞侵袭力，增强SKOV3和OVCAR3细胞对紫杉醇的敏感性。其作用机制与STAT3诱骗ODN对EMMPRIN、P-gp和PAKT的抑制有关。这三种蛋白可能是STAT3的靶蛋白。这些发现表明，STAT3是卵巢癌转移和化疗耐药的关键因素。STAT3诱骗ODN可能被证明是一种有益的治疗药物，特别是对侵袭性或化疗耐药的卵巢癌。(C)2010 Elsevier Inc.保留所有权利。
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. (C) 2010 Elsevier Inc. All rights reserved.