Open AccessUp-regulated Linc00472 suppresses development of lung cancer cell via inhibition of MiR-196b-5p
Author(s) -
XiaoMing Mao,
Xiaohu Zhou,
Jun Liu,
Yiran Mao,
Zhou Hua
Publication year - 2019
Publication title -
bioscience biotechnology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.509
H-Index - 116
eISSN - 1347-6947
pISSN - 0916-8451
DOI - 10.1080/09168451.2019.1694404
Subject(s) - apoptosis , flow cytometry , viability assay , western blot , cell migration , biology , cancer research , cell culture , gentamicin protection assay , cell , microbiology and biotechnology , chemistry , biochemistry , gene , genetics
The role of linc00472 in lung cancer (LC) has been rarely reported. We aimed to study the role of linc00472 in LC progression. Expressions of linc00472 and miR-196b-5p in LC cell lines were measured by qRT-PCR. The targeting relationship between linc00472 and miR-196b-5p was determined by Starbase and dual-luciferase reporter. The viability, migration, invasion, and apoptosis of LC cells were determined using CCK-8 assay, scratch test, transwell assay, and flow cytometry, respectively. The levels of epithelial-to-mesenchymal transition (EMT)-related proteins and apoptosis-related proteins in LC cells were determined by western blot. Down-regulated linc00472 was observed in five LC cell lines. Linc00472 overexpression suppressed viability, migration, invasion and EMT process, but elevated apoptotic rate in LC cells. MiR-196b-5p mimic promoted viability, migration, invasion, and EMT process, but decreased apoptotic rate, which was reversed by up-regulated linc00472. Linc00472 functioned as a cancer suppressor via negatively regulating miR-196b-5p of LC cells.
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