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...
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| Published in | Archives of biochemistry and biophysics Vol. 755; p. 109983 |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Elsevier Inc
01.05.2024
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| Abstract | 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.
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•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. |
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| AbstractList | 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. 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. |
| ArticleNumber | 109983 |
| Author | Jiao, Xinlin Hao, Chunyan Ye, Jinwen Hao, Yiping Gao, Qun Ma, Guangzhen Liu, Qingqing Wang, Bingyu Zhang, Teng Wang, Qi Cui, Baoxia Zhang, Wenjing |
| Author_xml | – sequence: 1 givenname: Qi surname: Wang fullname: Wang, Qi organization: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China – sequence: 2 givenname: Bingyu surname: Wang fullname: Wang, Bingyu organization: Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China – sequence: 3 givenname: Wenjing surname: Zhang fullname: Zhang, Wenjing organization: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China – sequence: 4 givenname: Teng surname: Zhang fullname: Zhang, Teng organization: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China – sequence: 5 givenname: Qingqing surname: Liu fullname: Liu, Qingqing organization: Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China – sequence: 6 givenname: Xinlin surname: Jiao fullname: Jiao, Xinlin organization: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China – sequence: 7 givenname: Jinwen surname: Ye fullname: Ye, Jinwen organization: Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China – sequence: 8 givenname: Yiping surname: Hao fullname: Hao, Yiping organization: Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, China – sequence: 9 givenname: Qun surname: Gao fullname: Gao, Qun organization: Department of Obstetrics and Gynecology, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao, 266000, Shandong, China – sequence: 10 givenname: Guangzhen surname: Ma fullname: Ma, Guangzhen organization: Department of Pathology, The Second People's Hospital of Liaocheng, Liaocheng, 252600, Shandong, China – sequence: 11 givenname: Chunyan surname: Hao fullname: Hao, Chunyan email: haochy@sdu.edu.cn organization: Department of Pathology, School of Basic Medical Sciences and Qilu Hospital, Shandong University, Jinan, Shandong Province, PR China – sequence: 12 givenname: Baoxia surname: Cui fullname: Cui, Baoxia email: cuibaoxia@sdu.edu.cn organization: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38561035$$D View this record in MEDLINE/PubMed |
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| Keywords | Glycolysis PI3K/AKT/mTOR pathway Proliferation Migration Cervical cancer APLN |
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| SubjectTerms | APLN Cervical cancer Glycolysis Migration PI3K/AKT/mTOR pathway Proliferation |
| Title | APLN promotes the proliferation, migration, and glycolysis of cervical cancer through the PI3K/AKT/mTOR pathway |
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