Identification of Shared Pathways and Molecules Between Type 2 Diabetes and Lung Adenocarcinoma and the Impact of High Glucose Environment on Lung Adenocarcinoma

Conclusion: The research established a shared pathogenic basis between LUAD and T2DM. TGF-β, HIF-1, AGE–RAGE, ECM components and function regulation, cell adhesion, and additional signaling pathways are intricately linked with the pathophysiological mechanisms underlying both LUAD and T2DM. Thus, ST...

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Bibliographic Details
Main Authors: Mengsi Yang, Jianmin Luo, Yunna Zheng, Qunqing Chen
Format: Article
Language:English
Published: Wiley 2025-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/ije/7734237
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Summary:Conclusion: The research established a shared pathogenic basis between LUAD and T2DM. TGF-β, HIF-1, AGE–RAGE, ECM components and function regulation, cell adhesion, and additional signaling pathways are intricately linked with the pathophysiological mechanisms underlying both LUAD and T2DM. Thus, STK26 may affect the development of LUAD and T2DM by regulating glucose metabolism. Suppressing STK26 in a glucose-rich setting curtailed both the expansion and mobility of LUAD cells.
ISSN:1687-8345