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Knockdown of Myosin 6 inhibits proliferation of oral squamous cell carcinoma cells
Author(s) -
Zhang Xinyu,
Huang Zhiquan,
Hu Yongjie,
Liu Liu
Publication year - 2016
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12448
Subject(s) - cell cycle , gene knockdown , apoptosis , cell growth , cell , biology , flow cytometry , small hairpin rna , western blot , cancer research , gene silencing , rna interference , microbiology and biotechnology , rna , biochemistry , gene
Background Oral squamous cell carcinoma ( OSCC ) accounts for 95% of all oral cancer with higher mortality and morbidity rates worldwide. However, the potential molecular mechanism of OSCC remains largely unclear. Myosin VI ( MYO 6 ) is a unique actin motor and reported to be overexpressed in several cancers. This study aims to examine the functional relationship between OSCC and MYO 6 . Methods The mRNA expression of MYO 6 was firstly investigated by analyzing data derived from Oncomine database. On the basis of the results, the expression of MYO 6 was knocked down using lentivirus‐delivered RNA interference in human OSCC cell line CAL 27, as confirmed by qPCR and Western blot analysis. Stable MYO 6 knockdown cells were employed to determine the effects of MYO 6 ‐silencing on cell growth by MTT , colony formation and cell cycle distribution and apoptosis by flow cytometry assay. Moreover, the expressions of cell apoptotic proteins were examined by Western blot analysis. Results We first observed MYO 6 was overexpressed in tongue squamous cell carcinoma TSCC belongs to OSCC , compared with normal tissues. For cellular analysis, sh RNA sequences against MYO 6 could efficiently reduce its expression in CAL 27 cells. Knockdown of MYO 6 significantly decreased cell proliferation, caused cell cycle arrest at G2/M phase, and promoted cell apoptosis. Moreover, cell apoptosis‐associated proteins, caspase‐3 and PARP , were obviously upregulated in CAL 27 after MYO 6 ‐silencing. Conclusion MYO 6 could play an essential role in the growth of OSCC cells via regulation of cell cycle progression and apoptosis.