Oncotarget

Research Papers:

This article has been corrected. Correction in: Oncotarget. 2018; 9:37268.

Verteporfin inhibits gastric cancer cell growth by suppressing adhesion molecule FAT1

Myoung-Hee Kang, Gi Seok Jeong, Duane T. Smoot, Hassan Ashktorab, Chang Mo Hwang, Byung Sik Kim, Hee Sung Kim _ and Yun-Yong Park

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:98887-98897. https://doi.org/10.18632/oncotarget.21946

Metrics: PDF 1985 views  |   HTML 4699 views  |   ?  


Abstract

Myoung-Hee Kang1,2, Gi Seok Jeong3, Duane T. Smoot4, Hassan Ashktorab5, Chang Mo Hwang3, Byung Sik Kim6, Hee Sung Kim6 and Yun-Yong Park1,2

1Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea

2Department of Convergence Medicine, University of Ulsan College of Medicine, Seoul, Republic of Korea

3Biomedical Engineering Research Center, Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea

4Department of Internal Medicine, Meharry Medical College, Nashville, TN, USA

5Department of Medicine and Cancer Center, Howard University, Washington, DC, USA

6Department of Gastric Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea

Correspondence to:

Hee Sung Kim, email: [email protected]

Yun-Yong Park, email: [email protected]

Keywords: verteporfin, gastric cancer, FAT1, metastasis

Received: July 12, 2017     Accepted: September 23, 2017     Published: October 19, 2017

ABSTRACT

Gastric cancer (GC) is a leading cause of death worldwide and in urgent need of targeted drug development. In the current, we investigated the ability of a repositioned drug verteporfin (VP), originally a treatment for macular degeneration, to inhibit GC cell growth. VP inhibited growth of various GC cell lines. Gene expression profiling of GC cell lines treated with VP revealed that migration-related genes and those with oncogenic potential were down-regulated. Of these genes, we found that FAT1, an adhesion molecule promoting cell invasion, was highly suppressed by VP. Silencing of FAT1 suppressed cell migration and invasion as VP did. FAT1 expression was up-regulated in tumors, and patients with high FAT1-expressing tumors had a worse prognosis. We propose that VP- targeting FAT1 to suppress metastatic potential is a promising therapeutic strategy against GC.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 21946