Verteporfin inhibits gastric cancer cell growth by suppressing adhesion molecule FAT1

34Citations
Citations of this article
15Readers
Mendeley users who have this article in their library.

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.

Cite

CITATION STYLE

APA

Kang, M. H., Jeong, G. S., Smoot, D. T., Ashktorab, H., Hwang, C. M., Kim, B. S., … Park, Y. Y. (2017). Verteporfin inhibits gastric cancer cell growth by suppressing adhesion molecule FAT1. Oncotarget, 8(58), 98887–98897. https://doi.org/10.18632/oncotarget.21946

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free