LncRNA TUC338 promotes invasion of lung cancer by activating MAPK pathway.

OBJECTIVE

Lung cancer is highly heterogeneous and the 5-year survival rate is less than 15%. It is currently difficult to determine the heterogeneity of lung cancer and the underlying pathogenetic of metastasis. We aimed to investigate the effect of long non-coding RNA (lncRNA) TUC338 on the invasion of lung cancer by activating MAPK pathway and to understand the heterogeneity and metastasis mechanism of lung cancer.

PATIENTS AND METHODS

The expression of lncRNA TUC338 in 42 samples of lung cancer and paracancerous tissues were accessed by RT-qPCR. The relationship between the expression of lncRNA and clinicopathological parameters was analyzed. After overexpressing and interfering with lncRNA TUC338, effects of lncRNA TUC338 on cell proliferation and invasion were determined by cell counting kit-8 (CCK8) and transwell assay. The protein expression was evaluated by Western blot.

RESULTS

Higher expression of TUC338 in lung cancer was observed in comparison with that in paracancerous tissues. The survival time of TUC338 was correlated with the expression of TUC338. Clinical data analysis revealed that the expression of TUC338 was correlated with the overall survival, tumor size and lymph node metastasis in patients, but not with age and gender. After interfering and overexpressing TUC338, it was found that the activity of lung cancer cells was decreased, as well as the invasion ability after interference with TUC338. After overexpression of TUC338, we found that lung cancer cell activity increased, as well as the invasion ability. By Western blot, we found that TUC338 can promote the development of lung cancer through regulating MAPK pathway.

CONCLUSIONS

TUC338 was overexpressed in lung cancer, and its expression may have a relationship to the prognosis of lung cancer. MAPK pathway was involved in the invasion of lung cancer regulated by TUC338.