Cordycepin Activates Autophagy to Suppress FGF9-induced TM3 Mouse Leydig Progenitor Cell Proliferation DOI Open Access
Su-Zhen Wu, Yu-Yan Lan,

Chia‐Fu Chen

и другие.

Cancer Genomics & Proteomics, Год журнала: 2024, Номер 21(6), С. 630 - 644

Опубликована: Окт. 28, 2024

Background/Aim: Fibroblast growth factor 9 (FGF9) is a member of the human FGF family known for its pivotal roles in various biological processes, such as cell proliferation, tissue repair, and male sex determination including testis formation. Cordycepin, bioactive compound found Cordyceps sinensis, exhibits potent antitumor effects by triggering apoptosis and/or autophagy pathways. Our research has unveiled that FGF9 promotes proliferation tumorigenesis MA-10 mouse Leydig tumor cells, phenomena are effectively countered cordycepin through induction. Moreover, we have observed FGF9-mediated stimulation TM3 progenitor prompting an investigation into potential inhibitory effect on under treatment. Hence, hypothesized induces death via FGF9-treated cells. Materials Methods: cells were treated with FGF9, flow cytometry, immunofluorescent plus western blotting assays used to determine how regulated Results: findings reveal restricts viability colony formation while inducing morphological alterations associated Surprisingly, fails elicit expression key apoptotic markers, suggesting alternate mechanism action. Although certain autophagy-related proteins remains unaltered, significant up-regulation LC3-II, indicative autophagy, cordycepin-treated influence. inhibition chloroquine reverses cordycepin-induced death, highlighting crucial role this process. Conclusion: study demonstrates activates induce treatment conditions.

Язык: Английский

Cordycepin Activates Autophagy to Suppress FGF9-induced TM3 Mouse Leydig Progenitor Cell Proliferation DOI Open Access
Su-Zhen Wu, Yu-Yan Lan,

Chia‐Fu Chen

и другие.

Cancer Genomics & Proteomics, Год журнала: 2024, Номер 21(6), С. 630 - 644

Опубликована: Окт. 28, 2024

Background/Aim: Fibroblast growth factor 9 (FGF9) is a member of the human FGF family known for its pivotal roles in various biological processes, such as cell proliferation, tissue repair, and male sex determination including testis formation. Cordycepin, bioactive compound found Cordyceps sinensis, exhibits potent antitumor effects by triggering apoptosis and/or autophagy pathways. Our research has unveiled that FGF9 promotes proliferation tumorigenesis MA-10 mouse Leydig tumor cells, phenomena are effectively countered cordycepin through induction. Moreover, we have observed FGF9-mediated stimulation TM3 progenitor prompting an investigation into potential inhibitory effect on under treatment. Hence, hypothesized induces death via FGF9-treated cells. Materials Methods: cells were treated with FGF9, flow cytometry, immunofluorescent plus western blotting assays used to determine how regulated Results: findings reveal restricts viability colony formation while inducing morphological alterations associated Surprisingly, fails elicit expression key apoptotic markers, suggesting alternate mechanism action. Although certain autophagy-related proteins remains unaltered, significant up-regulation LC3-II, indicative autophagy, cordycepin-treated influence. inhibition chloroquine reverses cordycepin-induced death, highlighting crucial role this process. Conclusion: study demonstrates activates induce treatment conditions.

Язык: Английский

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