Pathophysiologic mechanism of CMTM5 low expression in multiple myeloma progression.
10.3760/cma.j.issn.0253-2727.2019.01.011
- Author:
Yuan MA
1
;
Jing Fang SHI
1
;
Hui Ying QIU
2
;
Jing YUAN
2
;
Yang ZHANG
3
;
Peng ZHOU
1
;
Jing Jing XU
1
;
Qing Zhen HAN
1
Author Information
1. Center for Clinical Labrotary, the First Affiliated Hospital of Soochow University, Suzhou 215006, China.
2. Institute of Hematology of Jiangsu, Suzhou 215006, China.
3. Clinical Laboratory, the Second Affiliated Hospital of Anhui Medical Univercity, Hefei 230001, China.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Chemokine-like factor superfamily member 5;
DNA methylation;
Multiple myeloma
- MeSH:
Apoptosis;
Cell Line, Tumor;
Cell Proliferation;
Chemokines/genetics*;
Disease Progression;
Humans;
MARVEL Domain-Containing Proteins/genetics*;
Multiple Myeloma;
Transfection;
Tumor Suppressor Proteins/genetics*
- From:
Chinese Journal of Hematology
2019;40(1):58-62
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the mechanism of chemokine-like factor superfamily member (CMTM) 5 on the proliferation of multiple myeloma cells. Methods: RT-qPCR method was used to detect the expression and correlation of CMTM5, caspase3 and caspase9 in U266 after decitabine demethylation treatment; U266 transfected with pcDNA3.1 plasmid overexpressed CMTM5, then cell proliferation activity was detected by CCK-8 assay. Results: Compared with the control group, the low-dose demethylation treatment increased mRNA expression of CMTM5, caspase3, and caspase9 in U266, and showed a time-dependent (P<0.01). The up-trend of CMTM5, caspase3, and caspase9 in the high-demethylation drug treatment group was more significant and also showed time-dependent (P<0.001); There was a significant positive correlation between CMTM5 and caspase3 (r=0.937) and caspase9 (r=0.945) in each group (P<0.001). After transfection of U266 with the pcDNA3.1-CMTM5 plasmid, overexpression of CMTM5 inhibited the cell proliferation activity compared with the control and pcDNA3.1-vector group. Conclusion: Decitabine has a reductive effect on the low level of CMTM5 in U266 cells, and its recovery level is significantly positively correlated with caspase 3 and caspase9. Re-expression of CMTM5 inhibits the proliferative activity of U266.
