Background/Aim:
Some long non-coding RNAs (lncRNAs) have been found to significantly participate in the progression of TGCTs. In comparison to the normal testis, the TGCT tissues showed significantly decreased
CSNK1G2-AS1
expression, however, its effect on TGCTs and its mechanism are still unclear. The aim of this study is to investigate the effect of
CSNK1G2-AS1
on TGCTs and explore the mechanism underlying its effect on TGCTs.
Materials and Methods:
In this study, to evaluate the expression of
CSNK1G2-AS1
in tissue samples from TGCTs, the UCSC and GEPIA databases were applied and qRT-PCR was conducted. The Kaplan-Meier Plotter was applied to analyze the correlation between
CSNK1G2-AS1
methylation levels and the prognosis of TGCTs patients. The assays of MTS, clone formation, transwell, and flow cytometry were performed to investigate the effect of
CSNK1G2-AS1
overexpression on the proliferation, metastasis, and apoptosis of TGCT cells, respectively. Finally, western blotting was conducted to determine the expressions of the proteins associated with EMT and AKT.
Results:
Our study first found that, compared to the normal testis, TGCTs tissue showed significantly decreased
CSNK1G2-AS1
expression, and hypomethylation of
CSNK1G2-AS1
was significantly correlated with a better prognosis with TGCTs patients.
In vitro
, we found that overexpression of
CSNK1G2-AS1
dramatically promoted the clone formation, invasion, and migration of TGCT cells, but inhibited apoptosis. And
CSNK1G2-AS1
overexpression significantly decreased the expression of EMT-associated proteins ZO-1 but increased the expression and phosphorylation of AKT.
Conclusions:
CSNK1G2-AS1
may play an essential role in the pathogenesis and metastasis of TGCTs through the EMT- and AKT-mediated signal pathways.