Open AccessGATA6‑AS1 inhibits ovarian cancer cell proliferation and migratory and invasive abilities by sponging miR‑19a‑5p and upregulating TET2
Author(s) -
Hui Xu,
Xiao Wang,
Yinghong Zhang,
Wei Zheng,
Huijie Zhang
Publication year - 2021
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2021.12979
Subject(s) - gata6 , oncogene , biology , cell growth , cancer research , microrna , downregulation and upregulation , cell cycle , antisense rna , microbiology and biotechnology , molecular medicine , cell , transcription factor , gene expression , gene , genetics
GATA6 antisense RNA 1 (GATA6-AS1) has been reported to be involved in the progression of several types of cancer. In the present study, the role of GATA6-AS1 in ovarian cancer (OC) was explored. Reverse transcription quantitative PCR was used to detect the expression of GATA6-AS1, microRNA (miR)-19a-5p and tet methylcytosine dioxygenase 2 (TET2) in OC and adjacent normal tissues. Furthermore, OC cells with GATA-AS1 either knocked down or overexpressed were established. The Cell Counting Kit-8 assay was used to evaluate cell proliferation and a Transwell assay was used to assess the migratory and invasive abilities of OC cells. A dual luciferase reporter gene assay was used to determine whether GATA6-AS1 and miR-19a-5p, and miR-19a-5p and TET2, may interact with each other. The results demonstrated that GATA6-AS1 expression level was decreased in OC tissues and cells compared with control groups. In addition, GATA6-AS1 overexpression significantly inhibited the proliferation and migratory and invasive abilities of OC cells, whereas GATA6-AS1 downregulation had the opposite effects. Furthermore, GATA6-AS1 adsorbed miR-19a-5p to repress its expression and GTA6-AS1 indirectly upregulated TET2 expression. Taken together, the findings from this study suggested that GATA6-AS1 could inhibit the proliferation and migratory and invasive abilities of OC cells via regulation of the miR-19a-5p/TET2 axis.