[Pathophysiologic mechanism of CMTM5 low expression in multiple myeloma progression]

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.