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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.