Abstract 6320: Benfotiamine and fursultiamine prevent glioblastoma cells growth, invasion and migration

Abstract Glioblastoma is the most common malignant and aggressive brain tumor in adults. Recent advances in surgical techniques and adjuvant therapies have modestly improved the overall survival rate. Thus, there is a need for novel therapeutic approaches and preventive strategies to control glioblastoma. Lipophilic derivatives of vitamin B1 have been used for many health conditions due to their substantial antioxidant and anti-inflammatory properties. However, their chemopreventive effects in glioblastoma are not known. This study investigated the chemopreventive potential of benfotiamine and fursultiamine using glioblastoma cells. Human glioblastoma (U-87) cell lines grown in Eagle’s Minimum Essential Media (EMEM) were treated with various concentrations of benfotiamine and fursultiamine. Cell viability was determined by MTT assay in a time- and dose-dependent manner. Apoptotic cell death was determined by Annexin-V staining and live-dead cell assay kits. The expression of various pro-apoptotic and anti-apoptotic factors and other inflammatory factors, including Bad, Bax, Bcl-2, cIAP-1, cIAP-2, and procaspase 3, was determined using a human apoptosis antibody array. Our results suggest that benfotiamine and fursultiamine prevent the growth of U-87 cells in a dose- and time-dependent manner. Further, they prevented the invasion and migration of glioblastoma cells. They also elevated the caspase-3 activation and reduced the mitochondrial reactive oxygen species. These compounds also regulate the expression of various pro- and anti-apoptotic factors. These findings suggest vitamin B1 derivatives could prevent glioblastoma tumor growth by upregulating the caspase-3-mediated apoptotic signaling pathways. Next, we plan to inject glioblastoma cells into the athymic nude mice xenograft model and examine the growth of glioblastoma cells in the absence and presence of vitamin B1 derivatives. Citation Format: Breauna Keane, Swathi Senthil, Kota V. Ramana. Benfotiamine and fursultiamine prevent glioblastoma cells growth, invasion 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 XX.

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Journal
Cancer Research
Published
2025-04-21
DOI
https://doi.org/10.1158/1538-7445.am2025-6320
Primary Topic
Pharmacological Receptor Mechanisms and Effects
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article
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article

Abstract 6320: Benfotiamine and fursultiamine prevent glioblastoma cells growth, invasion and migration

Kota V. Ramana, Breauna Keane, Swathi Senthil
Cancer Research
Pharmacological Receptor Mechanisms and Effects
article

Abstract 6320: Benfotiamine and fursultiamine prevent glioblastoma cells growth, invasion and migration

Kota V. Ramana, Breauna Keane, Swathi Senthil
article en

Abstract

Abstract Glioblastoma is the most common malignant and aggressive brain tumor in adults. Recent advances in surgical techniques and adjuvant therapies have modestly improved the overall survival rate. Thus, there is a need for novel therapeutic approaches and preventive strategies to control glioblastoma. Lipophilic derivatives of vitamin B1 have been used for many health conditions due to their substantial antioxidant and anti-inflammatory properties. However, their chemopreventive effects in glioblastoma are not known. This study investigated the chemopreventive potential of benfotiamine and fursultiamine using glioblastoma cells. Human glioblastoma (U-87) cell lines grown in Eagle’s Minimum Essential Media (EMEM) were treated with various concentrations of benfotiamine and fursultiamine. Cell viability was determined by MTT assay in a time- and dose-dependent manner. Apoptotic cell death was determined by Annexin-V staining and live-dead cell assay kits. The expression of various pro-apoptotic and anti-apoptotic factors and other inflammatory factors, including Bad, Bax, Bcl-2, cIAP-1, cIAP-2, and procaspase 3, was determined using a human apoptosis antibody array. Our results suggest that benfotiamine and fursultiamine prevent the growth of U-87 cells in a dose- and time-dependent manner. Further, they prevented the invasion and migration of glioblastoma cells. They also elevated the caspase-3 activation and reduced the mitochondrial reactive oxygen species. These compounds also regulate the expression of various pro- and anti-apoptotic factors. These findings suggest vitamin B1 derivatives could prevent glioblastoma tumor growth by upregulating the caspase-3-mediated apoptotic signaling pathways. Next, we plan to inject glioblastoma cells into the athymic nude mice xenograft model and examine the growth of glioblastoma cells in the absence and presence of vitamin B1 derivatives. Citation Format: Breauna Keane, Swathi Senthil, Kota V. Ramana. Benfotiamine and fursultiamine prevent glioblastoma cells growth, invasion 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 XX.

Cancer ResearchVol. 85(8_Supplement_1)
Philadelphia College of Osteopathic Medicine (US)
Openalex Percentile: Top 93%
Pharmacological Receptor Mechanisms and Effects
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