LINC01117 inhibits invasion and migration of lung adenocarcinoma through influencing EMT process

Abstract

AbstractBackgroundStudying the mechanism of action of LincRNAs in lung adenocarcinoma (LUAD) is of great importance for an in-depth understanding of the molecular mechanism of lung adeno carcinogenesis and development.ObjectiveTo identify long-stranded non-coding RNAs that are specifically highly expressed in LUAD cells and to investigate their function in LUAD cells to provide new potential targets for targeting LUAD therapy.MethodsThis study used publicly available data downloaded from The Cancer Genome Atlas (TCGA) database. Construction of siRNA and overexpression plasmid-packed lentiviral constructs were used to knock down and increase the expression of LINC01117 in LUAD cells. The effect of LINC01117 on LUAD cell migration and invasion was verified by scratch assays and Transwell assays. Western blot assays were performed to verify the effect of knocking down LINC01117 expression on key proteins of the EMT process.ResultsLINC01117 expression was upregulated in LUAD tissues and cell lines. Clinical correlation and prognostic analyses showed that LINC01117 was associated with poorer clinical features (staging and N classification) and poorer prognosis and could be analyzed as an independent prognostic factor. Cell migration and invasion were significantly inhibited in the knockdown group compared to the control group; in contrast, cell migration and invasion were promoted in the overexpression group. The expression of N-cadherin and vimentin, molecular markers of the EMT process, was elevated in the overexpression group, and the expression of E-cadherin was decreased. Conclusions: LINC01117 was highly expressed in LUAD cells, and inhibition of LINC01117 expression significantly inhibited the migration and invasion of LUAD cells, while overexpression of LINC01117 significantly promoted the migration and invasion of LUAD cells, and may affect the migration ability of LUAD cells through the EMT process. It suggests that LINC01117 may play a key role in the occurrence and development of LUAD.