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

## TL;DR

This study shows that MPMCA, a caffeic acid derivative, inhibits prostate cancer metastasis by targeting EMT-related transcription factors Snail and Slug.

## Contribution

MPMCA is identified as a novel therapeutic candidate for metastatic prostate cancer through its regulation of Snail and Slug.

## Key findings

- MPMCA blocks prostate cancer cell migration and invasion without affecting cell viability.
- MPMCA suppresses EMT by modulating mesenchymal and epithelial markers.
- MPMCA reduces Snail and Slug expression and prostate cancer metastasis in vivo.

## 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.