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. |
关键词 | |
相关链接 | [来源记录] |
收录类别 | |
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).
|
条目包含的文件 | 条目无相关文件。 |
|
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论