尹虹, 刘玥, 郑文岭, et al. Effects of miRNA-196b overexpression on proliferation, apoptosis and survivin, Cox-2 expression of K562 cells[J]. China Oncology, 2013, 23(5): 341-346.
尹虹, 刘玥, 郑文岭, et al. Effects of miRNA-196b overexpression on proliferation, apoptosis and survivin, Cox-2 expression of K562 cells[J]. China Oncology, 2013, 23(5): 341-346. DOI: 10.3969/j.issn.1007-3969.2013.05.004.
Background and purpose: BCR-ABL fusion gene is considered to be the molecular pathological basis and an effective indicator for diagnosis
observation
prognosis
and monitoring of chronic myelogenous leukemia (CML). MiRNA-196b had low expression in acute myeloid leukemia and played an important role in the development of disease. BCR-ABL is the target gene of miRNA-196b in CML
miRNA-196b overexpression leaded to BCR-ABL down-regulation or silencing. Survivin is a downstream gene of BCR-ABL signal pathways. Various studies had showed that survivin and Cox-2 cooperative regulated of cell proliferation and apoptosis in variety of tumors. The purpose of this study was to investigate the effects of miRNA-196b overexpression on proliferation
apoptosis and surviving
Cox-2 mRNA expression of K562 cells. Methods: Three groups including K562-196b
K562-pLV and K562 control groups were set up in this study. The cell proliferation and apoptosis were measured by CCK-8 assay and Annexin V-PE
respectively. The expression of Cox-2 and survivin genes at the mRNA level were detected by Q-PCR. Results: The proliferation of K562 cells could be significantly inhibited by miRNA-196b overexpression; Compared of the three groups of apoptosis rate
K562-196b group was significantly higher than K562 group (P0.05). The expression of survivin gene in miRNA-196b was donwregulated (P0.05)
but the expression of Cox-2 gene in miRNA-196b group had no significant difference (P0.05). Conclusion: The miRNA-196b plays an important role in K562 cells proliferation inhibition and apoptosis; Overexpression of miRNA-196b can down-regulate survivin gene expression
and provide some basis for miRNA-196b as a therapeutic target for chronic myelogenous leukemia.