中文版 | English
Title

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

Author
Corresponding AuthorXu, Jinfeng; Dong, Fajin
Publication Years
2022
DOI
Source Title
ISSN
1568-0096
EISSN
1873-5576
Volume22Issue:10
Abstract
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.
Keywords
URL[Source Record]
Indexed By
Language
English
SUSTech Authorship
First ; Corresponding
Funding Project
[Natural Science Foundation of Shenzhen][JCYJ201908061-51807192]
WOS Research Area
Oncology
WOS Subject
Oncology
WOS Accession No
WOS:000863838700005
Publisher
ESI Research Field
PHARMACOLOGY & TOXICOLOGY
Data Source
Web of Science
Citation statistics
Cited Times [WOS]:0
Document TypeJournal Article
Identifierhttp://kc.sustech.edu.cn/handle/2SGJ60CL/405976
DepartmentShenzhen People's Hospital
Affiliation
Jinan Univ, Shenzhen Peoples Hosp, Affiliated Hosp 1,Southern Univ Sci & Technol, Dept Ultrasound,Clin Med Coll 2, Shenzhen 518020, Guangdong, Peoples R China
First Author AffilicationShenzhen People's Hospital
Corresponding Author AffilicationShenzhen People's Hospital
First Author's First AffilicationShenzhen People's Hospital
Recommended Citation
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).
Files in This Item:
There are no files associated with this item.
Related Services
Fulltext link
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Export to Excel
Export to Csv
Altmetrics Score
Google Scholar
Similar articles in Google Scholar
[Zhang, Lei]'s Articles
[Hu, Xuqiao]'s Articles
[Wu, Huaiyu]'s Articles
Baidu Scholar
Similar articles in Baidu Scholar
[Zhang, Lei]'s Articles
[Hu, Xuqiao]'s Articles
[Wu, Huaiyu]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Zhang, Lei]'s Articles
[Hu, Xuqiao]'s Articles
[Wu, Huaiyu]'s Articles
Terms of Use
No data!
Social Bookmark/Share
No comment.

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.