Conclusion
TGF-β1 may mediate lncRNA GAPLINC expression to promote NSCLC cell invasion and migration.
Methods
The study included 70 patients with NSCLC (39 males and 31 females, 33 to 68 years, 49.3 ± 6.4 years). RT-qPCR, transient cell transfections, measurement of in vitro cell migration and invasion abilities and western blot were carrying out during the research.
Purpose
The present study aims to investigate the involvement of lncRNA GAPLINC in non-small lung cancer (NSCLC). Patients and
Results
We showed that GAPLINC was up-regulated in NSCLC tissues and positively correlated with TGF-β1. In vitro cell experiment showed that over-expression of TGF-β1 significantly up-regulated the expression of GAPLINC, while over-expression of GAPLINC failed to affect TGF-β1. Follow-up study showed that high GAPLINC level in NSCLC tissue was closely correlated with poor survival rate of NSCLC patients. Over-expressions of TGF-β1 and GAPLINC resulted to accelerated migration and invasion of NSCLC cells. In addition, the silencing of GAPLINC siRNA attenuated the effect of TGF-β1 treatment.