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Lentivirus‐Mediated Silencing of Myosin VI Inhibits Proliferation and Cell Cycle Progression in Human Lung Cancer Cells
Author(s) -
Yu Hui,
Zhu Zhenghong,
Chang Jianhua,
Wang Jialei,
Shen Xiaoyong
Publication year - 2015
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.12528
Subject(s) - lung cancer , cell cycle , gene knockdown , cancer research , biology , cell growth , flow cytometry , cancer cell , gene silencing , cancer , a549 cell , cell , microbiology and biotechnology , apoptosis , pathology , medicine , biochemistry , genetics , gene
Myosin VI ( MYO 6) is a unique actin motor, which moves toward the pointed ends of actin filaments. In this study, we found that MYO 6 is overexpressed in lung cancer tissues and associated with lung cancer progression, particularly lymph node metastasis. To investigate its functions in lung cancer cells, we generated recombinant lentivirus taking sh RNA of MYO 6. Using two lung cancer cell lines, A549 and 95D, we found that Lv‐sh MYO 6 could infect lung cancer cells with high efficiency and downregulate MYO 6 on both mRNA and protein levels. After knockdown of MYO 6, the proliferation rates of lung cancer cells were decreased significantly. The colony‐formation ability of MYO 6‐silenced lung cancer cells was also impaired with reduced colony numbers and fewer cells per colony. Flow cytometry showed that cell cycle progression was stuck at the G 0 /G 1 phase, especially at the sub‐G 1 phase, which represents apoptotic cells. Moreover, knockdown of MYO 6 downregulated the phosphorylation of ERK 1/2. Further experiments using another sh RNA of MYO 6 confirmed the above results. These results suggest that MYO 6 is crucial in maintaining cell cycle and cell growth of lung cancer cells. MYO 6 may serve as a potential therapeutic target for lung cancer treatment.