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CTHRC1表达上调通过激活表皮生长因子受体(EGFR)信号通路促进人上皮性卵巢癌的侵袭。

Upregulated CTHRC1 promotes human epithelial ovarian cancer invasion through activating EGFR signaling.

作者信息

Ye Jun, Chen Wei, Wu Zhi-Yong, Zhang Jin-Hui, Fei He, Zhang Li-Wen, Wang Ya-Hui, Chen Ya-Ping, Yang Xiao-Mei

机构信息

The Fifth People's Hospital of Shanghai, Shanghai 200240, P.R. China.

Department of Gynecology, Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, P.R. China.

出版信息

Oncol Rep. 2016 Dec;36(6):3588-3596. doi: 10.3892/or.2016.5198. Epub 2016 Oct 24.

DOI:10.3892/or.2016.5198
PMID:27779718
Abstract

Epithelial ovarian cancer (EOC) is the major cause of deaths from gynecologic malignancies, and metastasis is the main cause of cancer related death. Collagen triple helix repeat containing-1 (CTHRC1) is a secreted protein that has the ability to inhibit collagen matrix synthesis. In this study, we found that high CTHRC1 expression was associated with poor prognosis of EOC. In vitro experiments showed that CTHRC1 promoted migration and invasion of ovarian cancer cells. CTHRC1 had no effect on ovarian cancer cells viability. Additionally, EGFR inhibitors reduced the promotion effects of CTHRC1 on EOC cell invasion. After silencing of CTHRC1, downregulated expression of phosphorylation of EGFR/ERK1/2/AKT was observed in ovarian cancer cells. Taken together, our results suggest a role for CTHRC1 in the progression of ovarian cancer and identified CTHRC1 as a potentially important predictor for human ovarian cancer prognosis.

摘要

上皮性卵巢癌(EOC)是妇科恶性肿瘤死亡的主要原因,而转移是癌症相关死亡的主要原因。含胶原蛋白三螺旋重复序列-1(CTHRC1)是一种具有抑制胶原蛋白基质合成能力的分泌蛋白。在本研究中,我们发现CTHRC1高表达与EOC的不良预后相关。体外实验表明,CTHRC1促进卵巢癌细胞的迁移和侵袭。CTHRC1对卵巢癌细胞的活力没有影响。此外,表皮生长因子受体(EGFR)抑制剂可降低CTHRC1对EOC细胞侵袭的促进作用。CTHRC1沉默后,在卵巢癌细胞中观察到EGFR/细胞外信号调节激酶1/2/蛋白激酶B(ERK1/2/AKT)磷酸化表达下调。综上所述,我们的结果表明CTHRC1在卵巢癌进展中发挥作用,并确定CTHRC1是人类卵巢癌预后的一个潜在重要预测指标。

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