Functional implications of PABPC1 in the development of ovarian cancer.
EMT
PABPC1
invasion and migration
ovarian carcinoma
proliferation
Journal
Open medicine (Warsaw, Poland)
ISSN: 2391-5463
Titre abrégé: Open Med (Wars)
Pays: Poland
ID NLM: 101672167
Informations de publication
Date de publication:
2021
2021
Historique:
received:
14
10
2020
revised:
17
12
2020
accepted:
27
03
2021
entrez:
24
5
2021
pubmed:
25
5
2021
medline:
25
5
2021
Statut:
epublish
Résumé
This research aimed to probe the expression characteristics of poly(A)-binding protein cytoplasmic 1 (PABPC1) and its role on the phenotype of ovarian cancer (OC) cells and to further investigate the possible underlying mechanism. The expression of PABPC1 was analyzed according to the data from gene expression omnibus, The Cancer Genome Atlas (TCGA) and Oncomine databases and the RNA sequencing data set from TCGA were downloaded for evaluating the prognostic values. We revealed that compared with the healthy samples, PABPC1 was upregulated in OC samples. High expression of PABPC1 had a connection with a shorter survival for patients with OC. Loss and gain of function assays revealed that silencing PABPC1 significantly suppressed the viability, invasion and migration of SK-OV-3 cells, while PABPC1 overexpression in A2780 cells showed the reverse outcomes. Moreover, Western blot demonstrated that silencing PABPC1 notably inactivated the epithelial-mesenchymal transition (EMT) process, while upregulation of PABPC1 promoted the mitigation of epithelial phenotype and the acquisition of mesenchymal phenotype. Taken together, PABPC1 was upregulated in OC cells and served as a carcinogene to promote the OC cell growth and invasion partly by modulating the EMT process, which implied that PABPC1 might be considered as a useful biomarker for OC therapeutics.
Identifiants
pubmed: 34027108
doi: 10.1515/med-2021-0278
pii: med-2021-0278
pmc: PMC8122461
doi:
Types de publication
Journal Article
Langues
eng
Pagination
805-815Informations de copyright
© 2021 Cong Feng et al., published by De Gruyter.
Déclaration de conflit d'intérêts
Conflict of interest: The authors have no conflicts of interest to declare.
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