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Published on: March 30, 2019
Knockdown of BMI-1 causes cell-cycle arrest and derepresses p16INK4a, HOXA9 and HOXC13 mRNA expression in HeLa cells
Fenghua Chen1, Yirong Li, Lin Wang
1Laboratory Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Road 1277#, 430022, Wuhan, Hubei, People's Republic of China.
Abstract:
The human oncogene B-cell-specific Moloney murine leukemia virus integration site 1 (BMI-1) is a member of the mammalian Polycomb group family. The overexpression of BMI-1 is associated with human malignancies. In this study, the effects of knockdown of BMI-1 by shRNA-mediated RNA interference on cell cycle and possible downstream targets in human cervical adenocarcinoma HeLa cells were investigated. As a result, when the shRNA plasmid was stably introduced into the cell line, the mRNA and protein of BMI-1 were specifically down-regulated, and the cells increased in the phase of G1 and cells in S phase significantly decreased by flow cytometric analysis; the knockdown of BMI-1 expression could lead to significant up-regulation of p16INK4a, HOXA9 and HOXC13 mRNA expression, but hTERT and HOXB4 mRNA expression did not change significantly. In conclusion, RNAi-mediated knockdown of BMI-1 expression can induce cell-cycle arrest and up-regulate p16INK4a, HOXA9 and HOXC13 in HeLa cells. Our results suggest that targeting BMI-1 might be a therapeutic potential for the treatment of cancer.
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