system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Apoptosis, Apoptosis Regulatory Proteins, Base Sequence, Carcinoma, Squamous Cell, Caspase 3, Cell Cycle, Cell Cycle Checkpoints, Cell Line, Tumor, Cell Proliferation, Gene Knockdown Techniques, Head and Neck Neoplasms, Humans, Myosin Heavy Chains, RNA, Messenger, RNA, Small Interfering, Squamous Cell Carcinoma of Head and Neck, Tongue Neoplasms, Tumor Cells, Cultured, Up-Regulation.
user
Does knockdown of Myosin 6 inhibit proliferation of oral squamous cell carcinoma cells? Context: 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 (MYO6) is a unique actin motor and reported to be overexpressed in several cancers. This study aims to examine the functional relationship between OSCC and MYO6. The mRNA expression of MYO6 was firstly investigated by analyzing data derived from Oncomine database. On the basis of the results, the expression of MYO6 was knocked down using lentivirus-delivered RNA interference in human OSCC cell line CAL27, as confirmed by qPCR and Western blot analysis. Stable MYO6 knockdown cells were employed to determine the effects of MYO6-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. We first observed MYO6 was overexpressed in tongue squamous cell carcinoma TSCC belongs to OSCC, compared with normal tissues. For cellular analysis, shRNA sequences against MYO6 could efficiently reduce its expression in CAL27 cells. Knockdown of MYO6 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 CAL27 after MYO6-silencing.
assistant
MYO6 could play an essential role in the growth of OSCC cells via regulation of cell cycle progression and apoptosis. Final Decision: yes