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Carvacrol Alleviates Prostate Cancer Cell Proliferation, Migration, and Invasion through Regulation of PI3K/Akt and MAPK Signaling Pathways
被引:64
|作者:
Luo, Yun
[1
]
Wu, Jie-Ying
[1
]
Lu, Min-Hua
[1
]
Shi, Zhi
[2
,3
]
Na, Ning
[4
]
Di, Jin-Ming
[1
]
机构:
[1] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Urol, Guangzhou 510630, Guangdong, Peoples R China
[2] Jinan Univ, Coll Life Sci & Technol, Natl Engn Res Ctr Genet Med, Dept Cell Biol, Guangzhou 510632, Guangdong, Peoples R China
[3] Jinan Univ, Coll Life Sci & Technol, Guangdong Prov Key Lab Bioengn Med, Inst Biomed,Natl Engn Res Ctr Genet Med, Guangzhou 510632, Guangdong, Peoples R China
[4] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Kidney Transplantat, Guangzhou 510630, Guangdong, Peoples R China
基金:
中国国家自然科学基金;
高等学校博士学科点专项科研基金;
关键词:
IN-VITRO;
TRP-PLIK;
CHANNELS;
INHIBITION;
ACTIVATION;
KINASE;
GROWTH;
ABCB1;
D O I:
10.1155/2016/1469693
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
TRPM7 is a potential therapeutic target for treatment of prostate cancer. In this study, we investigated the effects of nonselective TRPM7 inhibitor carvacrol on cell proliferation, migration, and invasion of prostate cancer PC-3 and DU145 cells. Our results showed that carvacrol blocked TRPM7-like currents in PC-3 and DU145 cells and reduced their proliferation, migration, and invasion. Moreover, carvacrol treatment significantly decreased MMP-2, p-Akt, and p-ERK1/2 protein expression and inhibited F-actin reorganization. Furthermore, consistently, TRPM7 knockdown reduced prostate cancer cell proliferation, migration, and invasion as well. Our study suggests that carvacrol may have therapeutic potential for the treatment of prostate cancer through its inhibition of TRPM7 channels and suppression of PI3K/Akt and MAPK signaling pathways.
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页数:11
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