Synergistic effects of oxypeucedanin and temozolomide on viability, proliferation, apoptosis, and migration of T98G malignant glioblastoma cells

Abderam, Amir; Yazdi, Parisa; Abbasinezhad-moud, Farzaneh; Shirazinia, Matin; Pouyamanesh, Ghazaleh; Shojaee, Maryam; Ardalan Moghadam Al, Fatemeh; Bahrami, Afsane

doi:10.22038/ajp.2025.26224

Synergistic effects of oxypeucedanin and temozolomide on viability, proliferation, apoptosis, and migration of T98G malignant glioblastoma cells

Articles in Press

Document Type : Original Research Article

Authors

¹ Student Research Committee, Birjand University of Medical Sciences, Birjand, 9717853577, Iran

² - Student Research Committee, Birjand University of Medical Sciences, Birjand, 9717853577, Iran

³ Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

⁴ 3- Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

⁵ Department of medical laboratory science, Mashhad branch, Islamic Azad University, Mashhad, Iran

⁶ Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran

⁷ Imam reza hospital

10.22038/ajp.2025.26224

Abstract

Objective: Glioblastoma multiforme (GBM), an aggressive
primary brain tumor, distinguished by an invasive growth
pattern and resistance to current therapeutic strategy. This study
investigates the potential of Oxypeucedanin (OP) as a natural
compound to induce apoptosis and inhibit proliferation in T98G
GBM cells, either alone or in combination with Temozolomide
(TMZ).
Materials and Methods: T98G cells were exposed to OP and TMZ
individually and in combination. Then, cell viability (MTT assay),
cell proliferation (using trypan blue), mRNA expression (qRTPCR), Cell cycle and apoptosis (flow cytometry), and migration
(wound healing assay) were evaluated.
Results: The viability assays revealed that both OP and less
potentially TMZ decreased cell viability in a time- and dosedependent manner. Notably, the combination of OP and TMZ
demonstrated synergistic effects, substantially enhancing apoptosis
rates while reducing proliferation, as evidenced by reduced cell
growth rates and altered cell cycle distribution towards G2/M arrest.
Additionally, gene expression analysis indicated increased Bax/Bcl2 ratios and decreased Ki-67 levels, suggesting enhanced apoptotic
susceptibility and lowered proliferation capacity. Furthermore, the
wound healing assay confirmed reduced migration in T98G cells,
particularly in the combination treatment group.
Conclusion: This study suggests the potential of OP as a
complementary therapeutic agent alongside TMZ for GBM
treatment.

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