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LncRNA CASC2 inhibits proliferation and migration of adenocarcinoma cells via miR‐4735‐3p and mTOR
Author(s) -
Luo Meng,
Kong Demiao,
Pei Dengke,
Jin Xing,
Liu Di
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28025
Subject(s) - adenocarcinoma , cancer research , biology , somatic cell , pi3k/akt/mtor pathway , suppressor , phenotype , lung cancer , cancer , long non coding rna , lung , disease , downregulation and upregulation , medicine , signal transduction , gene , microbiology and biotechnology , genetics
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.