J Cancer 2019; 10(4):874-884. doi:10.7150/jca.27635 This issue

Research Paper

MYH9 Promotes Growth and Metastasis via Activation of MAPK/AKT Signaling in Colorectal Cancer

Bin Wang1,2, Xiaolong Qi1, Jian Liu3,4, Rui Zhou4, Chuang Lin3,4, Junjie Shangguan5, Zhuoli Zhang5,6, Liang Zhao3,4✉, Guoxin Li1✉

1. Department of General Surgery, Nanfang Hospital, Southern Medical University, Guangdong provincial Engineering Technology Research Center of Minimally Invasive Surgery, Guangzhou, China.
2. Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
3. Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, P.R. China
4. Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, P.R. China
5. Department of Radiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA
6. Robert H. Lurie Comprehensive Cancer Center, Chicago, IL, 60611, USA

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
Wang B, Qi X, Liu J, Zhou R, Lin C, Shangguan J, Zhang Z, Zhao L, Li G. MYH9 Promotes Growth and Metastasis via Activation of MAPK/AKT Signaling in Colorectal Cancer. J Cancer 2019; 10(4):874-884. doi:10.7150/jca.27635. Available from https://www.jcancer.org/v10p0874.htm

File import instruction


The contractile protein MYH9 (non-muscle myosin IIA) is an actin-binding protein that plays a fundamental role in cell adhesion, migration, and division. However, its distinct role in colorectal cancer (CRC) still remains unidentified. In this study, we detected significant MYH9 overexpression in CRC samples compared with paired normal tissues using western blotting and tissue microarray immunohistochemistry (IHC). Moreover, analysis of patient clinical information demonstrated that MYH9 overexpression was strongly correlated with lymph node metastasis and poor overall survival. Endogenous overexpression of MYH9 enhanced the ability of cell proliferation and migration in vitro, and accelerated CRC growth in mouse models. Silencing of MYH9 revealed repressive effects on CRC cells in vitro and in vivo. Furthermore, primary biomechanics that involved MAPK/AKT signaling mediated epithelial-mesenchymal transition (EMT) was uncovered underlying MYH9 dependent cell behaviors. Collectively, our data showed that MYH9 significantly promoted tumorigenesis by regulating MAPK/AKT signaling, and was remarkably correlated with poor prognosis in CRC. MYH9 may thus be a novel biomarker and drug target in the diagnosis and treatment of CRC.

Keywords: MYH9, CRC, Cancer Metastasis, EMT, Tumor Biomarker.