Effects of miR-221 on cell proliferation and apoptosis of chronic myeloid leukemia K562 cells and its mechanism
10.3872/j.issn.1007-385x.2019.12.003
- VernacularTitle:miR-221对慢性粒细胞白血病K562细胞增殖和凋亡的影响及其作用机制
- Author:
YU Youyou
1
;
LI Bin
2
;
YAN Ting
3
;
ZHANG Changgeng
4
Author Information
1. Department of Laboratory Medicine, Harraison International Peace Hospital
2. Department of Nursing, Harraison International Peace Hospital
3. Return Visit Center, Harraison International Peace Hospital
4. Department of Laboratory Medicine，Harraison International Peace Hospital
- Publication Type:Journal Article
- Keywords:
miR-221;
chronic myeloid leukemia (CML);
apoptosis;
proliferation;
JAK-STAT signaling pathway
- From:
Chinese Journal of Cancer Biotherapy
2019;26(12):1311-1317
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of down-regulation of miR-221 on cell proliferation and apoptosis of chronic myeloid leukemia (CML) K562 cells and its related regulatory mechanism. Methods: K562 cells were divided into control group, miRNAnegative control (miR-NC) group, miR-221 inhibitor group, miR-221 inhibitor+ negative control siRNA(NC siRNA) group and miR-221 inhibitor+SOCS3 siRNA group. The cells in the control group received no additional treatment. Cells in miR-NC group and miR-221 inhibitor group were transfected with miR-NC and miR-221 inhibitor, respectively. Cells in miR-221 inhibitor+NC siRNA group and miR-221 inhibitor+SOCS3 siRNA group were transfected with NC siRNA and SOCS3 siRNA, respectively, on the basis of successful transfection with miR-221 inhibitor. The transfection efficiency of miR-221 inhibitor was identified by qPCR. Cell viability in each group was measured by CCK-8 assay. Apoptosis in each group was detected by Annexin V-FITC/PI staining using a flow cytometry. The protein expressions of SOCS3, p-JAK1, p-JAK2, p-STAT3 and survivin in each group were detected by WB. Results: Compared with the control group, miR-221 expression was significantly down-regulated in miR-221 inhibitor group (P<0.01), cell viability was significantly reduced at 48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly increased (P< 0.01), the expression of SOCS3 was significantly increased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly reduced (all P<0.01). Compared with miR-221 inhibitor group, cell viability was significantly increased at 24, 48 and 72 h after transfection (P<0.05 or P<0.01), the number of apoptotic cells was significantly decreased (P<0.01) and the expression levels of p-JAK1, p-JAK2, p-STAT3 and survivin were significantly increased in miR-221 inhibitor+SOCS3 siRNA group (all P< 0.01). Conclusion: Down-regulation of miR-221 inhibits proliferation and promotes apoptosis of K562 cells, the mechanism of which may be related with up-regulating SOCS3 expression to suppress JAK-STAT3 signaling pathway.
- Full text:20191203.pdf
