The inhibitory effect and molecular mechanism of 6-gingerol on human multiple myeloma cells
10.3969/j.issn.1006-5725.2024.23.003
- VernacularTitle:6-姜辣素对人多发性骨髓瘤细胞的抑制作用及分子机制
- Author:
Chunfang KONG
1
;
Anna LI
1
;
Bo KE
1
;
Weirong DING
1
;
Tingting LIU
1
;
Huan FU
1
;
Tingting ZHANG
1
;
Chenghao JIN
1
;
Mei WU
1
Author Information
1. 江西省人民医院(南昌医学院第一附属医院)血液内科(江西南昌 330006);江西省血液病重点实验室(江西南昌 330006)
- Publication Type:Journal Article
- Keywords:
multiple myeloma;
6-gingerol;
cell proliferation;
cell apoptosis;
signal pathway
- From:
The Journal of Practical Medicine
2024;40(23):3291-3297
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibitory effect and elucidate the molecular mechanism of 6-gingerol on human multiple myeloma cells.Methods The human multiple myeloma cell lines RPMI 8226 and ARH77 were cultured in vitro,followed by treatment with varying concentrations(50,100,200,300,400 μmol/L)of 6-gingerol.The inhibitory effect on cell proliferation was assessed using the CCK-8 assay.Flow cytometry was employed to evaluate cell apoptosis and cycle distribution.Additionally,qRT-PCR and Western blotting techniques were utilized to analyze gene and protein expression levels.Results The proliferation of RPMI 8226 and ARH77 cells was dose-and time-dependently inhibited by 6-gingerol,leading to the induction of apoptosis with statistically significant differences(P＜0.05).Further mechanistic investigations revealed that treatment with 6-gingerol arrested RPMI 8226 cells in the G0/G1 phase,resulting in a significant increase in Bax levels and a decrease in Bcl-2 mRNA and c-Myc mRNA levels(P＜0.05).Additionally,it significantly upregulated the expression of Bax,Cleaved-PARP,Cleaved-caspase3,P53,and p-AKT proteins while down regulating the expression of Bcl-2 protein(P＜0.05).Conclusions The compound 6-Gingerol exhibits inhibitory effects on the proliferation and induction of apoptosis in MM cells,as well as cell cycle arrest at the G0/G1 phase.Its mechanism of action is likely associated with the suppression of the AKT signaling pathway,downregulation of Bcl-2 family protein expression,and inhibition of c-Myc expression.
