Emerging studies have shown that the aberrant expression and function of lncRNAs are involved in carcinogenesis and the development of various cancers. The long noncoding RNA (lncRNA) JPX on the X chromosome is an activator of XIST and is a molecular switch for X-chromosome inactivation. However, the exact mechanism by which JPX acts in non-small cell lung cancer (NSCLC) is not well studied. Here, through integrating clinical data and a series of functional experiments, we found that lncRNA JPX expression is significantly upregulated in NSCLC tissues compared with that in paired adjacent normal tissues from two independent datasets and significantly associated with a poor survival and other malignant phenotypes (tumor stage, tumor volume) of NSCLC. Furthermore, we elucidated that JPX functions as an oncogene in NSCLC promoting cell proliferation and cell migration by affecting cell-cycle progression. Mechanistically, JPX upregulates cyclin D2(CCND2) expression in a competing endogenous RNA mechanism by interacting with miR-145-5p, thus provoking the development and progression of NSCLC. These findings reveal the mechanism of X-chromosome lncRNA JPX and its core regulatory circuitry JPX/miR-145-5p/CCND2 in the development and progression of NSCLC, which bring us closer to an understanding of the molecular drivers of NSCLC cancer.
Links zum Inhalt
Empfehlungen zum selben Thema automatisch vorgeschlagen von bX