The molecular mechanism of long non-coding ribonucleic acid (lncRNA) RUNX1-IT1 promotes the proliferation and stemness of lung cancer cells.

BACKGROUND

This study sought to explore the role of long non-coding ribonucleic acid (lncRNA) RUNX1-IT1 in lung cancer proliferation and cell stemness and clarify its molecular mechanism.

METHODS

Quantitative reverse transcription polymerase chain reaction was used to detect the expression levels of lncRNA RUNX1-IT1 in lung cancer cell lines and tissues. Cell Counting Kit 8, a plate cloning experiment, a cell suspension sphere-forming assay and a Transwell assay were used to identify the effects of lncRNA RUNX1-IT1 overexpression or down-expression on clone formation, cell progression, cell stemness, and invasion. Western blot was used to detect the expression of associated proteins that regulate cell invasion and stemness.

RESULTS

Low expression levels of lncRNA RUNX1-IT1 were detected in the cancerous lung cells and tissues. The overexpression of lncRNA RUNX1-IT1 significantly restricted the ability of cells to proliferate, produce clones, form spheres, and invade lung cancer cells, while the knockdown of lncRNA RUNX1-IT1 had the opposite effect. The findings of the Western blot assessment showed that the overexpression or knockdown of lncRNA RUNX1-IT1 significantly affected the expression of cluster of differentiation 44, cluster of differentiation 133, sex-determining region Y-box 2, octamer-binding transcription factor 4, and Nanog, and regulated the sphere-forming ability of cells. Additionally, the overexpression or knockdown of lncRNA RUNX1-IT1 regulated the invasion ability of cells by affecting expressions of E-cadherin, N-cadherin, and Vimentin.

CONCLUSIONS

The poor expression, overexpression, or knockdown of lncRNA RUNX1-IT1 affects the stemness and invasion ability of lung cancer cells.