Zhang Dan, Qiu Shuang, Wang Qi, Zheng Jianhua
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Oncol Rep. 2016 Jan;35(1):81-8. doi: 10.3892/or.2015.4356. Epub 2015 Oct 29.
Overexpression of transmembrane protease, serine 3 (TMPRSS3) has been detected in ovarian cancer. However, the molecular mechanisms of TMPRSS3 in ovarian cancer remain unclear. In the present study, we found that TMPRSS3 was significantly expressed in ovarian cancer cells. Overexpression of TMPRSS3 promoted the proliferation, invasion and migration of A2780 cells. Conversely, knockdown of TMPRSS3 in HO8910 cells inhibited the proliferation, invasion and migration. Furthermore, TMPRSS3 affected the expression levels of E-cadherin, vimentin and Twist. In addition, TMPRSS3 induced activation of ERK1/2 in ovarian cancer cells, and the ERK1/2 pathway was required for the TMPRSS3-mediated proliferation, invasion and migration of ovarian cancer cells. Finally, knockdown of TMPRSS3 inhibited ovarian cancer HO8910 cell growth and metastasis in vivo. Collectively, the present study suggests that TMPRSS3 plays a crucial role in the development and progression of ovarian cancer. Therefore, TMPRSS3 represents a potential therapeutic target of ovarian cancer.
在卵巢癌中已检测到跨膜蛋白酶丝氨酸3(TMPRSS3)的过表达。然而,TMPRSS3在卵巢癌中的分子机制仍不清楚。在本研究中,我们发现TMPRSS3在卵巢癌细胞中显著表达。TMPRSS3的过表达促进了A2780细胞的增殖、侵袭和迁移。相反,在HO8910细胞中敲低TMPRSS3可抑制其增殖、侵袭和迁移。此外,TMPRSS3影响E-钙黏蛋白、波形蛋白和Twist的表达水平。另外,TMPRSS3诱导卵巢癌细胞中ERK1/2的激活,并且ERK1/2通路是TMPRSS3介导的卵巢癌细胞增殖、侵袭和迁移所必需的。最后,敲低TMPRSS3可抑制卵巢癌HO8910细胞在体内的生长和转移。总的来说,本研究表明TMPRSS3在卵巢癌的发生和发展中起关键作用。因此,TMPRSS3是卵巢癌的一个潜在治疗靶点。