Open Access

ARTICLE

MYH11 Suppresses Colorectal Cancer Progression by Inhibiting Epithelial-Mesenchymal Transition via ZEB1 Regulation

Yuhang Jiang^#, Yijun Xu^#, Qi Zhu, Yingxia Wu, Zhe Wang, Shuang He, Shiyong Yu^*, Honggang Xiang^*

Department of General Surgery, Shanghai Pudong New Area People’s Hospital, Shanghai, 201299, China

* Corresponding Authors: Shiyong Yu. Email: ; Honggang Xiang. Email:
# These authors contributed equally to this work

(This article belongs to the Special Issue: Advances and Innovations in Colorectal Cancer Research and Treatment)

Oncology Research 2025, 33(9), 2379-2398. https://doi.org/10.32604/or.2025.063501

Received 16 January 2025; Accepted 04 June 2025; Issue published 28 August 2025

Abstract

Background: Colorectal cancer (CRC) is common and deadly, often leading to metastasis, challenging treatment, and poor outcomes. Understanding its molecular basis is crucial for developing effective therapies. Aims: This study aimed to investigate the role of Myosin Heavy Chain 11 (MYH11) in CRC progression, especially its effects on epithelial-mesenchymal transition (EMT) and cell behavior, and to explore its potential regulation by the EMT transcription factor zinc finger E-box binding homeobox 1 (ZEB1). Methods: Differential expression analysis was performed in the GSE123390 and TCGA-READ datasets, and 317 intersection genes were identified. The hub gene MYH11 was identified based on Protein-protein interaction (PPI) analysis and expression validation. The effects of MYH11 and the EMT transcription factor (ZEB1) on the behavior of CRC cells were investigated in vitro. Results: Bioinformatics research revealed that MYH11 was considerably downregulated in CRC samples as compared to normal samples. Overexpression of MYH11 inhibited the proliferation, migration, and invasion of CRC cells. Western blotting (WB) testing showed that MYH11 overexpression inhibited EMT by elevating E-cadherin levels while suppressing ZEB1, vimentin, and N-cadherin expressions. By contrast, overexpression of ZEB1 promoted EMT and enhanced migration, invasion, and proliferation of CRC cells. The negative impacts of MYH11 affecting EMT markers and cell behaviors were partially mitigated by co-overexpression of MYH11 and ZEB1, indicating that MYH11 regulates EMT and CRC progression through ZEB1. Conclusion: Our study shows MYH11 curbs CRC growth by blocking EMT and invasion, but ZEB1 overexpression reduces this effect. It uncovers key CRC pathways and suggests MYH11’s therapeutic potential.

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Supplementary Material

Supplementary Material File

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