PT - JOURNAL ARTICLE AU - KONO, TOSHIAKI AU - FUJIHARA, SHINTARO AU - OURA, KYOKO AU - IWAMA, HISAKAZU AU - FUJITA, KOJI AU - FUJITA, NAOKI AU - TAKUMA, KEI AU - ONO, MASAHIRO AU - NAMIMA, DAISUKE AU - YAMANA, HIROKI AU - CHIYO, TAIGA AU - KOBAYASHI, KIYOYUKI AU - KAMADA, HIDEKI AU - KOBARA, HIDEKI AU - ONO, MASAHUMI AU - NIKI, TOSHIRO AU - HIRASHIMA, MITSUOMI AU - MASAKI, TSUTOMU TI - Antitumor Effect of Galectin-9 on Cell Proliferation and Tumor Growth of Human Duodenal Adenocarcinoma Cells AID - 10.21873/anticanres.16562 DP - 2023 Aug 01 TA - Anticancer Research PG - 3769--3777 VI - 43 IP - 8 4099 - http://ar.iiarjournals.org/content/43/8/3769.short 4100 - http://ar.iiarjournals.org/content/43/8/3769.full SO - Anticancer Res2023 Aug 01; 43 AB - Background/Aim: Galectin-9 (Gal-9) induces tumor cell apoptosis in lymphoma and other malignant cell types. Duodenal adenocarcinoma is a rare malignancy, and there are insufficient data to determine a standard therapeutic approach. Here, we investigated the antitumor effect of Gal-9 in HuTu-80 duodenal adenocarcinoma cells. Materials and Methods: Cell proliferation was examined in HuTu-80 cells using a Cell Counting Kit-8 assay. Cell cycle analysis, apoptosis array, and microRNA expression analysis were performed to identify the effect of Gal-9 on HuTu-80 cells. The antitumor effect of Gal-9 was also examined using xenograft mouse models. Results: Gal-9 suppressed the proliferation of HuTu-80 via blockade of the G0 to G1 cell cycle transition. This blockade was accompanied by a strong decrease in cyclin D1 and phosphorylated Rb, suggesting a G1 arrest. Additionally, Gal-9 induced apoptosis, and the expression of cleaved caspase-3 was increased in Gal-9-treated HuTu-80 cells according to the apoptosis array. MiRNA microarrays revealed that Gal-9 altered the expression of miRNAs in HuTu-80 cells. Conclusion: These data demonstrate the therapeutic potential of Gal-9 and provide molecular mechanistic insights into its antitumor effect in HuTu-80 cells.