TMEM211 Promotes Tumor Progression and Metastasis in Colon Cancer

Author:

Chang Yung-Fu123,Wang Hsing-Hsang1,Shu Chih-Wen4ORCID,Tsai Wei-Lun5,Lee Cheng-Hsin1,Chen Chun-Lin6ORCID,Liu Pei-Feng137ORCID

Affiliation:

1. Department of Biomedical Science and Environmental Biology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan

2. Translational Research Center of Neuromuscular Diseases, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan

3. Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung 80708, Taiwan

4. Institute of BioPharmaceutical Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan

5. Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan

6. Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan

7. Center for Cancer Research, Kaohsiung Medical University, Kaohsiung 80708, Taiwan

Abstract

Colon cancer is the third most important cancer type, leading to a remarkable number of deaths, indicating the necessity of new biomarkers and therapeutic targets for colon cancer patients. Several transmembrane proteins (TMEMs) are associated with tumor progression and cancer malignancy. However, the clinical significance and biological roles of TMEM211 in cancer, especially in colon cancer, are still unknown. In this study, we found that TMEM211 was highly expressed in tumor tissues and the increased TMEM211 was associated with poor prognosis in colon cancer patients from The Cancer Genome Atlas (TCGA) database. We also showed that abilities regarding migration and invasion were reduced in TMEM211-silenced colon cancer cells (HCT116 and DLD-1). Moreover, TMEM211-silenced colon cancer cells showed decreased levels of Twist1, N-cadherin, Snail and Slug but increased levels of E-cadherin. Levels of phosphorylated ERK, AKT and RelA (NF-κB p65) were also decreased in TMEM211-silenced colon cancer cells. Our findings indicate that TMEM211 regulates epithelial–mesenchymal transition for metastasis through coactivating the ERK, AKT and NF-κB signaling pathways, which might provide a potential prognostic biomarker or therapeutic target for colon cancer patients in the future.

Funder

Ministry of Science and Technology

National Sun Yat-sen University-KMU Joint Research Project

Kaohsiung Medical University Research Center Grant

Publisher

MDPI AG

Subject

Microbiology (medical),Molecular Biology,General Medicine,Microbiology

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