Inhibition of long non-coding RNA TUG1 on gastric cancer cell transference and invasion through regulating and controlling the expression of miR-144/c-Met axis

Objective: To discuss the expression of long noncoding RNA TUG1(lnc RNA-TUG1) in gastric carcinoma(GC) and its effects on the transferring and invading capacity of gastric carcinoma cells. Methods: Forty cases of carcinoma tissue and para-carcinoma tissue were selected from GC patients who underwent surgical removal in Zhejiang Provincial Hospital of Chinese Traditional Medicine and Wenzhou Central Hospital from January, 2013 to December, 2014; the expressing level of lnc RNA-TUG1 in GC and para-C tissues was detected by applying the q RT-PCR technique. The correlation between lnc RNA-TUG1 expression and patients’ clinical data was classified and analyzed. SGC-7901 cells were transfected using lnc RNA-TUG1 specific si RNA. Changes of the transferring and invading capacity of si RNAtransfected SGC-7901 cells were scratch-tested and transwell-detected. q RT-PCR was applied to detect the expression level of micro RNA-144 after lnc RNA-TUG1 was silenced. Changes of c-Met m RNA and protein expressions was detected by q RT-PCR and western-blot test. Results: The expression level of lnc RNA-TUG1 in GC tissue was significant higher than that in para-C tissue(P<0.05) and the high expression level of lnc RNA-TUG1 in GC tissue was significantly correlated with tumor lymph nodes metastasis and advance TNM phasing(P<0.05). The transferring and invading capacity of SGC-7901 cells was highly inhibited after being transfected by lnc RNA-TUG1 specific si RNA(P<0.05). The results of q RT-PCR and western-blot proved that the expression of micro RNA-144 was significantly boosted and the expression level of c-Met m RNA and protein was inhibited after lnc RNA-TUG1 was silenced(P<0.05). Conclusions: lnc RNA-TUG1 shows an up-regulated expression in GC tissue and that bears a correlation with clinicopathological features of malignant tumor. lnc RNATUG1 can promote the transferring and invading capacity of GC by inhibiting the pathway of micro RNA-144/c-Met.