PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer

PLAC1 是生存率低的独立预测因子,并促进宫颈癌细胞增殖和侵袭

阅读:5
作者:Rujun Chen #, Chan Sheng #, Ruyue Ma, Liwen Zhang, Lina Yang, Yaping Chen

Abstract

Placenta‑specific protein 1 (PLAC1) is inversely associated with survival in several types of cancer. However, whether PLAC1 is involved in the progression of cervical cancer (CC) remains to be elucidated. Therefore, the present study aimed to evaluate the prognostic role of PLAC1 in CC by determining the relationship between clinicopathological factors, PLAC1 gene expression and survival prognosis using univariate and multivariate Cox proportional‑hazards regression analyses. Similarly, Kaplan‑Meier curves were evaluated with the log‑rank test. Subsequently, gene set enrichment analysis was performed to compare the high‑ and low‑PLAC1 expression phenotypes. Functional studies were further conducted in PLAC1‑overexpressing HeLa cells and PLAC1‑silenced MS751 cells, and western blotting was performed to determine whether PLAC1 promoted CC progression via epithelial‑mesenchymal transition (EMT). The findings demonstrated that high expression of PLAC1 was associated with American Joint Committee on Cancer metastasis pathological score and suggested a poor overall survival. 'mTOR complex 1 signaling', 'interferon α response' and 'hypoxia' were differentially enriched in the high‑PLAC1 phenotype. Furthermore, PLAC1 promoted the invasion of CC cells in vitro. E‑cadherin expression was decreased in the PLAC1‑overexpressing cells, accompanied by increased expression of the mesenchymal markers, Vimentin, MMP2 and Slug, and the opposite effects were observed in PLAC1‑silenced cells. Taken together, the present results indicated that high expression of PLAC1 was associated with poor survival and PLAC1 promoted metastasis via EMT in CC.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。