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Verteporfin inhibits gastric cancer cell growth by suppressing adhesion molecule FAT1

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 G...

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Detalles Bibliográficos
Autores principales: Kang, Myoung-Hee, Jeong, Gi Seok, Smoot, Duane T., Ashktorab, Hassan, Hwang, Chang Mo, Kim, Byung Sik, Kim, Hee Sung, Park, Yun-Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716775/
https://www.ncbi.nlm.nih.gov/pubmed/29228735
http://dx.doi.org/10.18632/oncotarget.21946
Descripción
Sumario: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.