Document Type : Original Research Article
Authors
1
Traditional and Complementary Medicine Research Center, Arak University of Medical Sciences, Arak, Iran
2
Department of Applied Cell Sciences, Faculty of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
3
Department of Orthopedic, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran
4
Department of Molecular Medicine and Biotechnology, Faculty of Medicine, Arak University of Medical Sciences, Arak, Iran
10.22038/ajp.2026.27771
Abstract
Objective: Shifts in the balance of Bcl-2 family proteins are known to contribute to tumor cell resistance to ABT-737. The present research therefore investigated the role of epigallocatechin-3-gallate(EGCG) in modulating Mcl-1 expression and its subsequent impact on the sensitivity of glioblastoma cells to ABT-737.
Materials and Methods: To assess treatment effects, we conducted a series of assays. Cell proliferation was measured using trypan blue exclusion and colony formation assays, while cytotoxicity was determined via the MTT assay. We evaluated cell migration with a wound healing assay and analyzed apoptosis through Hoechst 33342 staining, an ELISA cell death assay, and a caspase-3 activity assay. Additionally, Mcl-1 mRNA expression levels were quantified using qRT-PCR.
Results: The results showed that combination therapy with EGCG and ABT-737 significantly enhanced the potency of ABT-737, as evidenced by a marked reduction in its IC50 value. This treatment also synergistically suppressed colony formation, migration, survival, and growth of glioblastoma cells more effectively than either EGCG or ABT-737 alone. Specifically, EGCG treatment was found to significantly inhibit Mcl-1 mRNA expression. This downregulation of Mcl-1 was further associated with increased apoptosis induction by ABT-737.
Conclusion: EGCG exerts multiple anti-tumor effects, such as inhibiting colony formation, proliferation, and migration, while also activating the intrinsic apoptosis pathway. Furthermore, it can sensitize glioblastoma cells to ABT-737, an effect associated with the suppression of Mcl-1 mRNA expression.
Keywords
Main Subjects
)