Functional implications of PABPC1 in the development of ovarian cancer

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..

Medienart:

E-Artikel

Erscheinungsjahr:

2021

Erschienen:

2021

Enthalten in:

Zur Gesamtaufnahme - volume:16

Enthalten in:

Open Medicine - 16(2021), 1, Seite 805-815

Sprache:

Englisch

Beteiligte Personen:

Feng Cong [VerfasserIn]
Han Yan-Hua [VerfasserIn]
Qi Na [VerfasserIn]
Li Jia [VerfasserIn]
Sheng Qing-Hua [VerfasserIn]
Liu Yu [VerfasserIn]
Yang Li-Li [VerfasserIn]

Links:

doi.org [kostenfrei]
doaj.org [kostenfrei]
doi.org [kostenfrei]
Journal toc [kostenfrei]

Themen:

Emt
Invasion and migration
Medicine
Ovarian carcinoma
Pabpc1
Proliferation
R

doi:

10.1515/med-2021-0278

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

DOAJ032135815