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.
Keywords: Long non-coding ribonucleic acid RUNX1-IT1 (lncRNA RUNX1-IT1); cell proliferation; cycle block arrest; lung cancer; nude mice.
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