LncRNA CASC2 inhibits proliferation and migration of adenocarcinoma cells via miR‐4735‐3p and mTOR

Lung adenocarcinoma is a major form of non–small‐cell lung cancer that frequently strikes nonsmokers. The disease is often diagnosed at a late stage and the 5‐year survival rate is very low. Although previous studies found many somatic alterations associated with lung adenocarcinoma, the molecular basis of the development and progression of the disease is not well understood. We found that long noncoding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2), a putative tumor suppressor, was downregulated in both patient adenocarcinoma tissues and cultured lung cancer cells. Its tumor suppression function seemed to be dependent on its binding to miR‐4735‐5p. Changing the levels of CASC2 and miR‐4735‐3p in the cultured adenocarcinoma cells could affect the malignant phenotypes as well as growth of tumors derived from the cells injected into nude mice. Furthermore, the lncRNA and miR‐4735‐3p interplay likely the suppressed tumor growth through the downstream mammalian target of rapamycin signaling pathway. The results have revealed molecular details that may be critical for the development of lung adenocarcinoma, opening opportunities for the development of novel, and therapeutic tools. Cancer susceptibility candidate 2 and miR‐4735‐3p pair regulate proliferation and migration of adenocarcinoma cells via the mammalian target of rapamycin (mTOR)‐associated signaling. This further confirmed the critical role of this signaling molecule in the development of lung adenocarcinoma and thus justified the efforts in developing new drugs targeting the mTOR‐associated signaling network.