Caffeic Acid Derivative MPMCA Inhibits Prostate Cancer EMT and Metastasis by Regulating Transcription Factors Snail and Slug

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Authors: Jo-Yu Lin, Tien‐Huang Lin, Yuan-Li Huang, Chao-Yang Lai, Trung‐Loc Ho, Chun-Hao Tsai, Yi‐Chin Fong, Hsi-Chin Wu, An‐Chen Chang, Yueh-Hsiung Kuo, Sung‐Lin Hu, Chih‐Hsin Tang
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References: 57

Abstract

Prostate cancer (PCa) is the most general cancer in men and is often linked with distant metastasis in its later stages. The caffeic acid (CA) derivative, N-(4-methoxyphenyl)methylcaffeamide (MPMCA), demonstrates superior liver-protective effects compared to CA. Nevertheless, the functions of MPMCA on prostate cancer metastasis remain unclear. Here, we demonstrate that MPMCA blocks migration and invasion in prostate cancer cells without affecting cell viability. By suppressing the production of mesenchymal markers Vimentin, N-cadherin and β-catenin and upregulating the production of the epithelial marker Zonula Occludens-1 (ZO-1), MPMCA also controls Epithelial-Mesenchymal Transition (EMT). The Phosphoinositide 3-kinase (PI3K), Protein kinase B (AKT) and mechanistic target of rapamycin (mTOR) pathway has been documented to regulate MPMCA-inhibited cell motility. Transfection with Snail and Slug cDNA reverses MPMCA's suppression of EMT, migration, and invasion in prostate cancer cells. Importantly, our in vivo data indicates that MPMCA reduces Snail and Slug expression and prostate cancer metastasis. Our evidence suggests that MPMCA is a novel therapeutic candidate for treating metastatic prostate cancer.

Fields of Study & Subjects

Cancer Cells and Metastasis Prostate Cancer Treatment and Research Mechanisms of cancer metastasis

Publication details

Journal / source
Cells
Volume
15
Issue
5
Pages
454–454
Publication date
3 March 2026
Language
EN