Objective: Long non-coding RNAs (lncRNAs) have been identified to participate in the development and progression of various types of cancers, including non-small cell lung cancer (NSCLC). However, the expression and function of linc00261 in NSCLC has not been studied yet. We aim to explore the role and potential of linc00261 in NSCLC tumorigenesis.
Patients and methods: The expression level of linc00261 in 71 paired of NSCLC tissues and matched normal tissues, was detected using quantitative Real-time polymerase chain reaction (qRT-PCR). Linc00261 expression in NSCLC cells was also measured. NSCLC cells were transfected with pcDNA3.1 or siRNA linc00261 to upregulate or downregulate linc00261 expression, respectively. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and colony formation assay were utilized for examining the proliferative ability of NSCLC cells. Wound-healing and transwell assays were performed for detecting the metastatic ability of NSCLC cells. Protein levels of epithelial-mesenchymal transition markers were detected by Western blot. Furthermore, in vivo function of linc00261 was evaluated using the nude mice.
Results: Linc00261 expressed significantly lower in NSCLC tissues and cell lines than that in the adjacent normal tissues or control cell line. Over-expression of linc00261 significantly inhibited proliferation, invasion and migration of NSCLC cells. On the contrast, knockdown of linc00261 promoted cell growth and metastasis of NSCLC cells. Furthermore, linc00261 inhibited the epithelial-mesenchymal transition of NSCLC via downregulating Snail. Linc00261 could slow down the growth of xenograft of NSCLC in vivo.
Conclusions: We demonstrated that linc00261 was lowly expressed in NSCLC tissues and cells. It inhibited cell proliferation and metastasis by downregulating Snail expression via EMT. This might provide a novel sight for the biological treatment for NSCLC.