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tRF‐Leu‐CAG promotes cell proliferation and cell cycle in non‐small cell lung cancer
Author(s) -
Shao Yang,
Sun Qiangling,
Liu Xiaomin,
Wang Ping,
Wu Renqi,
Ma Zhongliang
Publication year - 2017
Publication title -
chemical biology and drug design
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 77
eISSN - 1747-0285
pISSN - 1747-0277
DOI - 10.1111/cbdd.12994
Subject(s) - carcinogenesis , biology , cell growth , cancer research , gene knockdown , cell cycle , lung cancer , downregulation and upregulation , cell , rna , cell culture , microbiology and biotechnology , gene , pathology , medicine , genetics
tRNA ‐derived RNA fragments ( tRF s), non‐coding single‐stranded RNA s with 14–35 nt in length, were found to play important roles in gene regulation, even in carcinogenesis. In this study, we investigated the expression of tRF ‐Leu‐ CAG in human non‐small cell lung cancer ( NSCLC ) and its function in the cell proliferation and cell cycle of NSCLC . The expression level of tRF ‐Leu‐ CAG was detected in NSCLC tissues, cell lines, and sera. tRF ‐Leu‐ CAG RNA levels were higher in NSCLC tumor tissues than in normal tissues, and also upregulated in NSCLC cell lines. A significant relationship was observed between stage progression and tRF ‐Leu‐ CAG in NSCLC sera. We found that in H1299 cells, inhibition of tRF ‐Leu‐ CAG suppressed cell proliferation and impeded cell cycle. AURKA was also repressed with the knockdown of tRF ‐Leu‐ CAG . Thus, our study revealed that tRF ‐Leu‐ CAG may be involved in regulating AURKA and could be a new diagnostic marker and potential therapeutic target in NSCLC.