RT Journal Article
SR Electronic
T1 Indoleamine 2,3-Dioxygenase Inhibitor Suppresses Colon Cancer Cell Migration, Invasion, and Epithelial-Mesenchymal Transition
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3337
OP 3342
DO 10.21873/anticanres.17153
VO 44
IS 8
A1 YOKOTA, YUMI
A1 NOZAWA, HIROAKI
A1 SONODA, HIROFUMI
A1 YOKOYAMA, YUICHIRO
A1 EMOTO, SHIGENOBU
A1 MURONO, KOJI
A1 SASAKI, KAZUHITO
A1 ISHIHARA, SOICHIRO
YR 2024
UL http://ar.iiarjournals.org/content/44/8/3337.abstract
AB Background/Aim: Indoleamine 2,3-dioxygenase 1 (IDO1) is a key enzyme in tryptophan metabolism and plays an important role in immunosuppression. The effects of IDO1 on tumor invasion and metastasis have been studied in several types of malignancies. However, the role of IDO1 in these steps in colorectal cancer (CRC) has not been elucidated. Therefore, we aimed to investigate the effects of IDO1 on invasion, migration, and epithelial–mesenchymal transition (EMT) in CRC cells. Materials and Methods: All experiments were performed using the DLD-1 colon cancer cell line that expresses IDO1. We conducted a scratch wound healing assay and Boyden chamber assay to investigate the impact of IDO1 on DLD-1 cell migration and invasion, respectively, in the presence and absence of the IDO1 inhibitor L-1-methyl-tryptophan (L-1-MT). Additionally, western blotting was performed to analyze alterations in the expression of EMT-related markers caused by L-1-MT. Results: High expression of IDO1 was confirmed in the cytoplasm of DLD-1 by immunofluorescence staining. In the scratch wound healing assay, the invasion ability of DLD-1 cells decreased to 62% after treatment with L-1-MT at 1,000 μM for 24 h. In the Boyden chamber assay, the migration of DLD-1 cells was suppressed by 85% after treatment with L-1-MT at 2,500 μM for 24 h. L-1-MT treatment increased the expression level of E-cadherin and decreased the expression levels of vimentin, Snail, and Slug. Conclusion: IDO1 inhibition reduced the invasion and migration ability of IDO1-expressing DLD-1 colon cancer cells, which was accompanied by altered expression of EMT-related proteins. IDO1 could be a potential target for the treatment of advanced CRC.