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RhoC在卵巢癌细胞上皮-间质转化中的作用。

The role of RhoC in epithelial-to-mesenchymal transition of ovarian carcinoma cells.

作者信息

Gou Wen-feng, Zhao Yang, Lu Hang, Yang Xue-feng, Xiu Yin-ling, Zhao Shuang, Liu Jian-min, Zhu Zhi-tu, Sun Hong-zhi, Liu Yun-peng, Xu Feng, Takano Yasuo, Zheng Hua-chuan

机构信息

Cancer Research Center, The First Affiliated Hospital of Liaoning Medical University, 121001 Jinzhou, China.

出版信息

BMC Cancer. 2014 Jul 1;14:477. doi: 10.1186/1471-2407-14-477.

DOI:10.1186/1471-2407-14-477
PMID:24986540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4226981/
Abstract

BACKGROUND

RhoC is a small G protein/GTPase and involved in tumor mobility, invasion and metastasis. Previously, up-regulated RhoC expression is found to play an important role in ovarian carcinogenesis and subsequent progression by modulating proliferation, apoptosis, migration and invasion.

METHODS

We transfected RhoC-expressing plasmid and RhoC siRNA into CAOV3 and OVCAR3 cells respectively. These cells and transfectants were exposed to vascular epithelial growth factor (VEGF), transforming growth factor (TGF)-β1 or their receptor inhibitors with the phenotypes and their related-molecules examined.

RESULTS

TGF-β1R or VEGFR inhibitor suppressed the proliferation, migration, invasion and lamellipodia formation, the expression of N-cadherin, α-SMA, snail and Notch1 mRNA or protein, and enhanced E-cadherin mRNA and protein expression in CAOV3 and its RhoC-overexpressing transfectants, whereas both growth factors had the opposite effects in OVCAR3 cells and their RhoC-hypoexpressing transfectants. Ectopic RhoC expression enhanced migration, invasion, lamellipodia formation and the alteration in epithelial to mesenchymal transition (EMT) markers of CAOV3 cells regardless of the treatment of VEGFR or TGF-β1R inhibitor, whereas RhoC knockdown resulted in the converse in OVCAR3 cells even with the exposure to VEGF or TGF-β1.

CONCLUSION

RhoC expression might be involved in EMT of ovarian epithelial carcinoma cells, stimulated by TGF-β1 and VEGF.

摘要

背景

RhoC是一种小G蛋白/GTP酶，参与肿瘤的移动、侵袭和转移。此前研究发现，RhoC表达上调通过调节增殖、凋亡、迁移和侵袭，在卵巢癌发生及后续进展中发挥重要作用。

方法

我们分别将表达RhoC的质粒和RhoC小干扰RNA转染至CAOV3和OVCAR3细胞。将这些细胞及转染细胞暴露于血管内皮生长因子（VEGF）、转化生长因子（TGF）-β1或其受体抑制剂，检测其表型及相关分子。

结果

TGF-β1受体或VEGF受体抑制剂抑制了CAOV3及其RhoC过表达转染细胞的增殖、迁移、侵袭和片状伪足形成，以及N-钙黏蛋白、α-平滑肌肌动蛋白、蜗牛蛋白和Notch1 mRNA或蛋白的表达，并增强了E-钙黏蛋白mRNA和蛋白的表达，而这两种生长因子在OVCAR3细胞及其RhoC低表达转染细胞中则产生相反的作用。无论是否用VEGF受体或TGF-β1受体抑制剂处理，异位表达RhoC均增强了CAOV3细胞的迁移、侵袭、片状伪足形成及上皮-间质转化（EMT）标志物的改变，而在OVCAR3细胞中，即使暴露于VEGF或TGF-β1，敲低RhoC也会产生相反的结果。

结论

RhoC表达可能参与了由TGF-β1和VEGF刺激的卵巢上皮癌细胞的EMT过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/9be1535ae4c9/1471-2407-14-477-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/8f8cc661aee1/1471-2407-14-477-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/da7019f142b0/1471-2407-14-477-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/2ece166abed5/1471-2407-14-477-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/7dc158dfe19c/1471-2407-14-477-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/590f44865176/1471-2407-14-477-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/9be1535ae4c9/1471-2407-14-477-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/8f8cc661aee1/1471-2407-14-477-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/da7019f142b0/1471-2407-14-477-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/2ece166abed5/1471-2407-14-477-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/7dc158dfe19c/1471-2407-14-477-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/590f44865176/1471-2407-14-477-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cc8/4226981/9be1535ae4c9/1471-2407-14-477-6.jpg

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