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题名

Knockdown of ARL5B Induces Mitochondrial-mediated Apoptosis and Inhibits Glycolysis in Breast Cancer Cells by Activating MDA5 Signaling

作者
通讯作者Xu, Jinfeng; Dong, Fajin
发表日期
2022
DOI
发表期刊
ISSN
1568-0096
EISSN
1873-5576
卷号22期号:10
摘要
Aim: Mitochondria are essential for energy metabolism in the tumor microenvironment and the survival of cancer cells. Background: ADP-ribosylation factor-like GTPase 5b (ARL5B) has been found to be associated with mitochondrial dysfunction and breast cancer (BC) progression, but the underlying mechanism needs to be further understood. Objective: We investigated the effects of ARL5B on the apoptosis and glycolysis of breast cancer cells and its underlying mechanisms. Methods: Quantitative reverse transcription-PCR (qRT-PCR) and western blot assays were used to detect the expression of ARL5B in breast cancer tissues and cells. An ARL5B loss-of-function assay was performed to verify its role in BC development. Results: ARL5B was upregulated in breast cancer tissues and cell lines. ARL5B knockdown induced apoptosis and activated the mitochondrial pathway in breast cancer cells. Interestingly, the inhibition of ARL5B repressed the aerobic glycolysis of breast cancer cells. The role of ARL5B in breast cancer cells was exerted by mediating the activation of viral RNA sensor MDA5-evoked signaling. Silencing ARL5B triggered MDA5 signaling by upregulating the key proteins involved in the MDA5 pathway. Importantly, MDA5 silencing reversed the effects of ARL5B knockdown on mitochondrial-mediated apoptosis and glycolysis, whereas poly (I:C), as a ligand for MDA5, further enhanced ARL5B knockdown-facilitated mitochondrial apoptosis and the inhibition of glycolysis. Conclusion: The knockdown of ARL5B activated MDA5 signaling and thus led to the enhanced mitochondrial-mediated apoptosis and glycolysis inhibition in breast cancer cells. Our study suggested that ARL5B might be a potential therapy target for BC.
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语种
英语
学校署名
第一 ; 通讯
资助项目
[Natural Science Foundation of Shenzhen][JCYJ201908061-51807192]
WOS研究方向
Oncology
WOS类目
Oncology
WOS记录号
WOS:000863838700005
出版者
ESI学科分类
PHARMACOLOGY & TOXICOLOGY
来源库
Web of Science
引用统计
被引频次[WOS]:0
成果类型期刊论文
条目标识符http://sustech.caswiz.com/handle/2SGJ60CL/405976
专题南方科技大学第一附属医院
作者单位
Jinan Univ, Shenzhen Peoples Hosp, Affiliated Hosp 1,Southern Univ Sci & Technol, Dept Ultrasound,Clin Med Coll 2, Shenzhen 518020, Guangdong, Peoples R China
第一作者单位南方科技大学第一附属医院
通讯作者单位南方科技大学第一附属医院
第一作者的第一单位南方科技大学第一附属医院
推荐引用方式
GB/T 7714
Zhang, Lei,Hu, Xuqiao,Wu, Huaiyu,et al. Knockdown of ARL5B Induces Mitochondrial-mediated Apoptosis and Inhibits Glycolysis in Breast Cancer Cells by Activating MDA5 Signaling[J]. CURRENT CANCER DRUG TARGETS,2022,22(10).
APA
Zhang, Lei.,Hu, Xuqiao.,Wu, Huaiyu.,Tian, Hongtian.,Zeng, Jieying.,...&Dong, Fajin.(2022).Knockdown of ARL5B Induces Mitochondrial-mediated Apoptosis and Inhibits Glycolysis in Breast Cancer Cells by Activating MDA5 Signaling.CURRENT CANCER DRUG TARGETS,22(10).
MLA
Zhang, Lei,et al."Knockdown of ARL5B Induces Mitochondrial-mediated Apoptosis and Inhibits Glycolysis in Breast Cancer Cells by Activating MDA5 Signaling".CURRENT CANCER DRUG TARGETS 22.10(2022).
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