Long noncoding RNA PCAT‐1 knockdown prevents the development of ovarian cancer cells via microRNA‐124‐3p

Long noncoding RNA prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT‐1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of P...

Full description

Saved in:
Bibliographic Details
Published in:Journal of cellular biochemistry Vol. 121; no. 2; pp. 1963 - 1972
Main Authors: Min, Fengying, Chu, Guoyan
Format: Journal Article
Language:English
Published: United States 01.02.2020
Subjects:
Apoptosis
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Cell Movement
Cell Proliferation
Female
Gene Expression Regulation, Neoplastic
Humans
MicroRNAs - genetics
miR‐124‐3p
ovarian cancer
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
PCAT‐1
RNA, Long Noncoding - genetics
Tumor Cells, Cultured
PCAT-1
apoptosis
miR-124-3p
ovarian cancer
ISSN:0730-2312, 1097-4644, 1097-4644
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Long noncoding RNA prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human malignancies and its silence abates the exaggeration of cancers. Whereas, the activity of PCAT‐1 silence in ovarian cancer (OC) remains elusive. Here, our study was designed to corroborate the function of PCAT‐1 silence in cellular activities and the molecular mechanisms. PCAT‐1 in human ovarian tumor tissue specimens and cell lines (A2780 and SKOV3) were quantified by real‐time quantitative reverse polymerase chain reaction (qRT‐PCR). Reinforced silence of PCAT‐1 and microRNA (miR)‐124‐3p was established by transfection and identified by qRT‐PCR. The viability, apoptosis as well as migration and invasion were examined. Western blot was exploited for analysis of proteins involved in proliferation, apoptosis, migration and invasion, and signaling transduction. OC tissues showed the accumulation of PCAT‐1. Silencing PCAT‐1 caused the impediment of proliferation, migration, and invasion with the increase in apoptosis. PCAT‐1 knockdown repressed the expression of cyclin D1, CDK6, p53, Bax, cleaved caspase‐3, metallopeptidases, and vimentin with the restoration of miR‐124‐3p. However, the roles of PCAT‐1 silence were weakened in the absence of miR‐124‐3p. PCAT‐1 silence caused decrease in Wnt3a, β‐catenin, and phosphorylation of protein kinase B and mechanistic target of rapamycin was abolished by miR‐124‐3p inhibitor. The tumor‐suppressive role of PCAT‐1 silence was mediated by miR‐124‐3p. Prostate cancer‐associated transcript 1 (PCAT‐1) is overexpressed in human ovarian tumor tissue specimens; PCAT‐1 silence represses the growth of ovarian cancer cells dependent on microRNA (miR)‐124‐3p; Wnt and protein kinase B/AKT/mechanistic target of rapamycin pathways are blocked by PCAT‐1 silence‐induced miR‐124‐3p.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Correction/Retraction-3
ISSN:0730-2312
1097-4644
1097-4644
DOI:10.1002/jcb.29431