MiR-301a/b function as oncomiRs in non-small-cell lung cancer

Abstract

Non-small-cell lung cancer (NSCLC) is one of the leading causes of cancer death worldwide. Although recent advances in understanding the pathogenic mechanism of NSCLC has led to the development of targeted treatments, these treatments are only applicable to a limited number of patients. Therefore, the development of a novel therapeutic drug for NSCLC is urgently needed. Here, we focused on miR-301a and miR-301b, belonging to the miR-130 family, because recently, it was reported that miR-130b functions as an oncomiR in NSCLC. The miR-301a and miR-301b were significantly upregulated in NSCLC tissues compared to those in matched-pair adjacent normal lung tissues. Overexpression of miR-301a/b promoted cell proliferation and miR-301b further promoted migration ability in NSCLC cells. Conversely, knockdown of miR-301a and miR-301b significantly suppressed cell proliferation and migration. Moreover, transactivating domain-containing p63 (TAp63), a close relative of the p53 tumor suppressor, was a target gene of both miR-301a and miR-301b in NSCLC cells. These findings showed that miR-301a and miR-301b might function as oncomiRs by targeting TAp63 in NSCLC. Abbreviations: NSCLC: non-small-cell lung cancer; miRNA: microRNA; 3’-UTR: 3’untranslated region; oncomiR: oncogenic miRNA; TAp63: transactivating domain-containing p63.