Lung cancer is the most common cause of cancer-related death in the world. Long non-coding RNAs (lncRNAs) are longer than 200 nucleotides transcripts which are not translated into protein. Linc00662 is overexpressed in lung cancer. However, the roles of linc00662 involved in lung cancer progression are still unknown. In our study, we found that linc00662 was overexpressed in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) by analyzing the TCGA data. We knockdown the linc00662 expression using siRNAs and found that silencing linc00662 significantly inhibited the proliferation and colony formation of A549 and H460 cells. We further found that knockdown of linc00662 increased the miR-145-5p expression and decreased PAFAH1B2 expression. We further showed that linc00662 could bind with miR-145-5p, and miR-145-5p could bind to the 3’UTR of PAFAH1B2. miR-145-5p could negatively regulate PAFAH1B2 both in the mRNA and protein levels. Loss of miR-145-5p could abolish the inhibitory effects of silencing linc00662 on the proliferation and colony formation of A549 and H460 cells. All these findings revealed that linc00662 functioned as an oncogene by acting as competing endogenous RNA (ceRNA) to sponge and regulate miR-145-5p in lung cancer and may provide a potential target of lung cancer treatment.
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