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

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 determini...

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Autores principales: Chen, Rujun, Sheng, Chan, Ma, Ruyue, Zhang, Liwen, Yang, Lina, Chen, Yaping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8456314/
https://www.ncbi.nlm.nih.gov/pubmed/34523695
http://dx.doi.org/10.3892/mmr.2021.12440
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author Chen, Rujun
Sheng, Chan
Ma, Ruyue
Zhang, Liwen
Yang, Lina
Chen, Yaping
author_facet Chen, Rujun
Sheng, Chan
Ma, Ruyue
Zhang, Liwen
Yang, Lina
Chen, Yaping
author_sort Chen, Rujun
collection PubMed
description 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.
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spelling pubmed-84563142021-09-29 PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer Chen, Rujun Sheng, Chan Ma, Ruyue Zhang, Liwen Yang, Lina Chen, Yaping Mol Med Rep Articles 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. D.A. Spandidos 2021-11 2021-09-14 /pmc/articles/PMC8456314/ /pubmed/34523695 http://dx.doi.org/10.3892/mmr.2021.12440 Text en Copyright: © Chen et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Chen, Rujun
Sheng, Chan
Ma, Ruyue
Zhang, Liwen
Yang, Lina
Chen, Yaping
PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
title PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
title_full PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
title_fullStr PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
title_full_unstemmed PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
title_short PLAC1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
title_sort plac1 is an independent predictor of poor survival, and promotes cell proliferation and invasion in cervical cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8456314/
https://www.ncbi.nlm.nih.gov/pubmed/34523695
http://dx.doi.org/10.3892/mmr.2021.12440
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