The long non-coding RNA CASC7 inhibits growth and invasion of non-small cell lung cancer cells through phosphatase and tensin homolog upregulation via sequestration of miR-92a

Accumulating evidence has demonstrated the crucial roles of long non-coding RNAs (lncRNAs) in various human cancers, including non-small cell lung cancer (NSCLC). However, to the best of our knowledge, the role of the lncRNA cancer susceptibility candidate 7 (CASC7) in NSCLC has not been clearly determined. The aim of the present study was to investigate the involvement of CASC7 in NSCLC. Marked downregulation of CASC7 was observed in NSCLC tissues and cell lines, and this downregulation of CASC7 was closely associated with distant metastasis, lymph node involvement and poor overall survival in NSCLC patients. Furthermore, overexpression of CASC7 significantly suppressed the proliferation, invasion and migration of the NSCLC cells A549 and H358, and promoted cell apoptosisin vitro. In addition, CASC7 was shown to act as a competing endogenous RNA by sponging miR-92a, which was proven to be an oncogenic miRNA in our previous study. The expression of miR-92a was upregulated in NSCLC tissues and cell lines, and was found to be inversely associated with CASC7 expression in NSCLC tissues. It was also demonstrated that CASC7 upregulated the expression of the tumor suppressor gene phosphatase and tensin homolog (a well-known target of miR-92a) by sequestration of miR-92a. Moreover, the tumor-suppressive effects of CASC7 were partly reversed by miR-92a overexpression in NSCLC cells. Collectively, the results of the present study indicated that CASC7 may act as a tumor-suppressive lncRNA that inhibits NSCLC progression by sponging miR-92a. These findings may improve our understanding of the potential mechanisms through which gain of CASC7 expression represses NSCLC progression.