Abstract 6322: Lipid-soluble vitamin B1 derivatives prevent pancreatic cancer growth and migration

Abstract Pancreatic adenocarcinoma is a lethal type of cancer often diagnosed in the end stages, commonly leading to metastasis. Surgical resection and chemotherapy are not well curative, leading patients to seek alternative therapies via clinical trials. Lipid-soluble derivatives of thiamine, Benfotiamine (Ben), and Fursultiamine (FS) exhibit antioxidative and anti-inflammatory properties. However, their chemo-preventive efficacy is not well known. Therefore, we examined their chemo-preventive potential in pancreatic cancer cells. Human Pancreatic adenocarcinoma (MIA PaCa-2) and metastatic pancreatic adenocarcinoma (BxPC-3) cell lines were incubated for 24 h with varying concentrations (0-100 uM) of Ben and FS. Cell viability was determined by MTT assay. Our results indicate that both Ben and FS prevented the growth of MIA-PaCa2 and BxPC-3 cells in a time- and dose-dependent manner. Ben and FS treatments also increased the expression of caspase-3 and prevented the invasion and trans-well migration of pancreatic cancer cells. Further, human apoptosis array analysis indicates that Ben regulated the expression of various pro-apoptotic factors such as BAD and Bax and anti-apoptotic factors such as Bcl-xL and Bcl-2 in MIA PaCA-2 cells. In addition, human oncology array analysis indicates that Ben regulated the expression of various carcinogenic proteins such as amphiregulin, cathepsin D, HIF-1alpha, osteopontin, p27, and Kallikrein. Next, we planned to examine the in-vivo chemo-preventive efficacy of Ben using nude mice xenografts. So far, our data suggests that treatment with vitamin B1 derivatives is effective against pancreatic cancer cell growth in culture. Citation Format: Nathan Kobus, Nancy Kaushal, Kota V. Ramana. Lipid-soluble vitamin B1 derivatives prevent pancreatic cancer growth and migration [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 6322.