APLN promotes the proliferation, migration, and glycolysis of cervical cancer through the PI3K/AKT/mTOR pathway

Apelin (APLN) is an endogenous ligand of the G protein-coupled receptor APJ (APLNR). APLN has been implicated in the development of multiple tumours. Herein, we determined the effect of APLN on the biological behaviour and underlying mechanisms of cervical cancer. The expression and survival curves...

Full description

Saved in:
Bibliographic Details
Published inArchives of biochemistry and biophysics Vol. 755; p. 109983
Main Authors Wang, Qi, Wang, Bingyu, Zhang, Wenjing, Zhang, Teng, Liu, Qingqing, Jiao, Xinlin, Ye, Jinwen, Hao, Yiping, Gao, Qun, Ma, Guangzhen, Hao, Chunyan, Cui, Baoxia
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.05.2024
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Apelin (APLN) is an endogenous ligand of the G protein-coupled receptor APJ (APLNR). APLN has been implicated in the development of multiple tumours. Herein, we determined the effect of APLN on the biological behaviour and underlying mechanisms of cervical cancer. The expression and survival curves of APLN were determined using Gene Expression Profiling Interactive Analysis. The cellular functions of APLN were detected using CCK-8, clone formation, EdU, Transwell assays, flow cytometry, and seahorse metabolic analysis. The underlying mechanisms were elucidated using gene set enrichment analysis and Western blotting. APLN was upregulated in the samples of patients with cervical cancer and is associated with poor prognosis. APLN knockdown decreased the proliferation, migration, and glycolysis of cervical cancer cells. The opposite results were observed when APLN was overexpressed. Mechanistically, we determined that APLN was critical for activating the PI3K/AKT/mTOR pathway via APLNR. APLN receptor inhibitor ML221 reversed the effect of APLN overexpression on cervical cancer cells. Treatment with LY294002, the PI3K inhibitor, drastically reversed the oncological behaviour of APLN-overexpressing C-33A cells. APLN promoted the proliferation, migration, and glycolysis of cervical cancer cells via the PI3K/AKT/mTOR pathway. [Display omitted] •APLN and APLNR are upregulated in cervical cancer tissues and cells.•APLN silencing suppressed cervical cancer cell proliferation, migration, and invasion.•APLN-regulated glycolysis in cervical cancer.•APLN/APLNR activated the PI3K/AKT/mTOR pathway in cervical cancer.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0003-9861
1096-0384
DOI:10.1016/j.abb.2024.109983