LINC00961 functions as an anti-oncogene in non-small cell lung carcinoma by regulation of miR-3127.

BACKGROUND

This study set out to explore the regulatory relationship between LINC00961/miR-3127 axis and non-small-cell lung carcinoma (NSCLC), so as to provide a new and effective molecular target for targeted therapy of NSCLC.

METHODS

RNA-seq and miRNA-seq data of NSCLC and normal samples were obtained from The Cancer Genome Atlas (TCGA) database for analyzing LINC00961 and miR-3127 expression. Eighty-six pairs of clinical NSCLC tissues and adjacent normal tissues as well as NSCLC cell lines were obtained. Measurements of LINK00961 and miR-3127 levels were done using real-time-quantitative polymerase chain reaction (RT-qPCR). Furthermore, LINK00961 and miR-3127 in NSCLC cell were regulated respectively. The NSCLC cell proliferation, invasion and migration were determined with MTT assay, Transwell and wound healing assays, respectively. The levels of invasion- and apoptosis-related proteins were detected using western blots, and the connection of LINC00961 and miR-3127 was identified using dual luciferase reporter (DLR) assay.

RESULTS

Differential analysis results of TCGA databases identified that LINC00961 was ubiquitously expressed at low levels in NSCLC, while miR-3127 was highly expressed. Similar expression trends of LINC00961 and miR-3127 were observed in clinical NSCLC samples and cell lines. Overexpression of LINC00961 and knockdown of miR-3127 significantly reduced NCI-H1299 cell migration, invasiveness, and multiplication, decreased MMP-2, MMP-9 and Bcl-2 protein levels, and increased E-cadherin, Bax and Caspase-3 protein levels. The DLR assay confirmed that miR-3127 can be targeted by LINC00961.

CONCLUSION

LINC00961 functions as an anti-oncogene in NSCLC by modulating miR-3127.