LINC00958 accelerates cell proliferation and migration in non-small cell lung cancer through JNK/c-JUN signaling.

Abstract

Non-small cell lung cancer (NSCLC) denotes the commonest type of lung cancers with high mortality globally. Long non-coding RNAs (lncRNAs) with differential expression have been indicated to be participants in the pathogenesis and development of cancer. However, the precise role of lncRNAs in NSCLC is still largely obscure. In this study, we explored a newly-discovered intergenic lncRNA LINC00958 in NSCLC. First of all, the online databases suggested that LINC00958 was low expressed in human normal lung tissues but upregulated in LUSC tissues. Besides, the upregulation of LINC00958 in both LUAD and LUSC cell lines was easily found when comparing to the normal BEAS-2B cells. In addition, we elucidated that knockdown of LINC00958 led to impaired proliferation, induced apoptosis and hampered migration in LUAD cells. Moreover, a typical oncogenic pathway, JNK signaling, was verified to be involved in LINC00958-contributed LUAD development. Of note, we explained that LINC00958 exerted the tumor-promoting function in LUAD by enhancing the transactivation of p-c-JUN through activating JNK signaling. Meanwhile, we also revealed that LINC00958 was transcriptionally regulated by c-JUN. Additionally, above findings were also suitable for LUSC cells. By and large, our work illustrated that LINC00958 facilitates tumorigenesis in NSCLC by activating JNK/c-JUN signaling pathway, indicating a new road for diagnosis and treatment of both LUAD and LUSC.