Yasuhide Muto1,2, Tomomi Furihata2, Meika Kaneko2, Kosuke Higuchi2, Kentaro Okunushi2, Hanae Morio2, Yoshie Reien2, Masaya Uesato1, Hisahiro Matsubara1, Naohiko Anzai3,4. 1. Department of Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Japan. 2. Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan. 3. Department of Pharmacology, Chiba University Graduate School of Medicine, Chiba, Japan anzai@chiba-u.jp. 4. Department of Pharmacology and Toxicology, Dokkyo Medical University School of Medicine, Tochigi, Japan.
Abstract
BACKGROUND/AIM: L-type amino acid transporter 1 (LAT1) is a promising molecular target for cancer therapy. The present study aimed to characterize the anti-cancer effects of JPH203, an LAT1-selective inhibitor, on gastrointestinal cancer cells. MATERIALS AND METHODS: Three esophageal, two gastric, and two colon cancer cell lines were used. Cytotoxic effects of JPH203 were assessed by a WST-8 assay. LAT1 mRNA levels were determined by quantitative PCR. The inhibitory property of JPH203 against LAT1 function was examined by a transport assay. RESULTS: JPH203 treatment significantly reduced the viability of all gastric and colon cancer cells. While LAT1 expression levels and inhibitory potencies of JPH203 on LAT1 functions were comparable among the cells, all the esophageal cells were resistant to JPH203. CONCLUSION: JPH203 was effective in reducing gastric and colon cancer cells. To clarify its cell type-dependent efficacy, identification of the causal factors for JPH203 resistance will be needed. Copyright
BACKGROUND/AIM: L-type amino acid transporter 1 (LAT1) is a promising molecular target for cancer therapy. The present study aimed to characterize the anti-cancer effects of JPH203, an LAT1-selective inhibitor, on gastrointestinal cancer cells. MATERIALS AND METHODS: Three esophageal, two gastric, and two colon cancer cell lines were used. Cytotoxic effects of JPH203 were assessed by a WST-8 assay. LAT1 mRNA levels were determined by quantitative PCR. The inhibitory property of JPH203 against LAT1 function was examined by a transport assay. RESULTS:JPH203 treatment significantly reduced the viability of all gastric and colon cancer cells. While LAT1 expression levels and inhibitory potencies of JPH203 on LAT1 functions were comparable among the cells, all the esophageal cells were resistant to JPH203. CONCLUSION:JPH203 was effective in reducing gastric and colon cancer cells. To clarify its cell type-dependent efficacy, identification of the causal factors for JPH203 resistance will be needed. Copyright