MDK Activates the PI3K/AKT Axis to Induce AP2A1 Expression and Epithelial–Mesenchymal Transition in Colorectal Cancer

MDK promotes invasion, migration, proliferation, metastasis, and EMT in CRC cells through the PI3K/AKT pathway by inducing AP2A1 expression, which could serve as a diagnostic marker. The PI3K inhibitor LY294002 significantly reduces AP2A1 levels and inhibits MDK-induced malignant behaviors. Targeting MDK-related signaling pathways may offer new strategies for CRC treatment.

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Publication Details

Journal
Cancers
Published
2026-04-21
DOI
https://doi.org/10.3390/cancers18081311
Primary Topic
Proteoglycans and glycosaminoglycans research
Type
article
Field-Weighted Citation Impact
0.00

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MDK Activates the PI3K/AKT Axis to Induce AP2A1 Expression and Epithelial–Mesenchymal Transition in Colorectal Cancer

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Cancers
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MDK Activates the PI3K/AKT Axis to Induce AP2A1 Expression and Epithelial–Mesenchymal Transition in Colorectal Cancer

Kaiji Chen, Chengyuan Xu, Tengfei Li, Jianming Zhang, Moubin Lin, Yunsheng Cheng, Yanyan Xu, Kesavamoorthy Gandhervin, Yang Guo
article en

Abstract

MDK promotes invasion, migration, proliferation, metastasis, and EMT in CRC cells through the PI3K/AKT pathway by inducing AP2A1 expression, which could serve as a diagnostic marker. The PI3K inhibitor LY294002 significantly reduces AP2A1 levels and inhibits MDK-induced malignant behaviors. Targeting MDK-related signaling pathways may offer new strategies for CRC treatment.

CancersVol. 18(8)
Tongji University (CN), Anhui Medical University (CN), Fudan University (CN), Pudong Medical Center (CN), Obstetrics and Gynecology Hospital of Fudan University (CN), Second Affiliated Hospital of Anhui Medical University (CN), Hangzhou Medical College (CN), University of Hong Kong (HK)
National Natural Science Foundation of China, Science and Technology Commission of Shanghai Municipality
No poverty
Openalex Percentile: Top 16%
Proteoglycans and glycosaminoglycans research
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