Down-regulation of HDAC6 Expression Can Influence KG1α Cell Proliferation by Inhibiting ERK Pathway.
10.7534/j.issn.1009-2137.2020.01.017
- Author:
Ze-Hong LIU
1
;
Bing GUO
1
;
Guan-Hai QIN
1
;
Zhi LI
1
;
Yan-Hua HOU
2
Author Information
1. Chongqing Engineering Research Center of Pharmaceutical Sciences, Chongqing Medical and Pharmaceutical College, Chongqing 401331, China.
2. Chongqing Engineering Research Center of Pharmaceutical Sciences, Chongqing Medical and Pharmaceutical College, Chongqing 401331, China,E-mail: liuliuliu20160520@163.com.
- Publication Type:Journal Article
- From:
Journal of Experimental Hematology
2020;28(1):98-103
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the inhibitory effect of HDAC6 on proliferation of human leukemia KG1α and to explore its mechanism by ERK signaling pathways.
METHODS:.The siRNA interference technology was used to inhibit the HDAC6 gene expression; the expression of HDAC6 and prateins of ERK signal pathway was detected by Western blot; the cell proliferation ability was detected by colony forming experiment and trypan blue staining; cell cycle was detected by FCM; and the expression of Ki67 was detected by immunofluorescence.
RESULTS:Western blot showed that HDAC6 expression was up-regulated in leukemia cell lines in comparison with the healthy volunteers and bone marrow stromal cells (P＜0.05). Knockdown of HDAC6 significantly inhibited the proliferation and colony formation ability of leukemia cells, promoted cell arrest at G/G phase. The Western blot and immunefluorescence showed that knockdown of HDAC6 suppressed the expression level of Ki67, CDK4, Cyclin D1 and enhanced the expression level of p16, p21, p-ERK (P＜0.05).
CONCLUSION:Knockdown of HDAC6 significantly inhibits the proliferation, arrest the cell cycle at G/G phase, and its mechanism probably relates with the activation of ERK signaling pathway.
