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MYCT 1 represses apoptosis of laryngeal cancerous cells through the MAX /miR‐181a/ NPM 1 pathway
Author(s) -
Wang HeTan,
Tong Xue,
Zhang ZhaoXiong,
Sun YuanYuan,
Yan Wei,
Xu ZhenMing,
Fu WeiNeng
Publication year - 2019
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.14942
Subject(s) - apoptosis , cancer cell , viability assay , cancer , microrna , cancer research , intracellular , microbiology and biotechnology , biology , chemistry , gene , genetics
MYCT 1 is an important gene known to regulate cell viability and apoptosis of laryngeal cancer cells. However, the underlying molecular mechanism remains unclear. Here, we show that MAX enhances the expression of miR‐181a by directly binding to its promoter, whereas miR‐181a targets NPM 1 and suppresses its expression in laryngeal cancer cells. MYCT 1 and miR‐181a decrease cell viability and colony formation through enhanced apoptosis, whereas NPM 1 displays opposite effects in laryngeal cancer cells. Their opposing functions are further supported by the findings (a) that miR‐181a is down‐regulated, while NPM 1 is up‐regulated in laryngeal cancer, and (b) that either inhibition of miR‐181a or overexpression of NPM 1 can revert the pro‐apoptotic effects of MYCT 1 on laryngeal cancer cells through extracellular and intracellular apoptotic pathways. Our data suggest that MYCT 1 may synergistically interact with MAX as a co‐transcription factor or a component of MAX transcriptional complex, to transcriptionally regulate the expression of miR‐181a , which, in turn, decreases NPM 1 expression at post‐transcriptional levels, leading to enhanced apoptosis in laryngeal cancer cells. These factors may serve as potential targets for early diagnosis and treatment of laryngeal cancer.