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

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

PMC · DOI: 10.22038/ajp.2025.26224 · 2025-11-01

## TL;DR

This study shows that combining oxypeucedanin with temozolomide can effectively reduce the growth and spread of glioblastoma cells.

## Contribution

The study demonstrates the synergistic effect of oxypeucedanin and temozolomide in treating glioblastoma cells.

## Key findings

- Oxypeucedanin and temozolomide combination significantly reduced cell viability and proliferation.
- The combination treatment increased apoptosis and caused G2/M cell cycle arrest in T98G cells.
- Gene expression analysis showed increased Bax/Bcl-2 ratios and reduced Ki-67 levels with combination treatment.

## Abstract

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).

T98G cells were exposed to OP and TMZ individually and in combination. Then, cell viability (MTT assay), cell proliferation (using trypan blue), mRNA expression (qRT-PCR), Cell cycle and apoptosis (flow cytometry), and migration (wound healing assay) were evaluated.

The viability assays revealed that both OP and less potentially TMZ decreased cell viability in a time- and dose-dependent 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/Bcl-2 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.

This study suggests the potential of OP as a complementary therapeutic agent alongside TMZ for GBM treatment.

## Linked entities

- **Genes:** BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596], Mki67 (antigen identified by monoclonal antibody Ki 67) [NCBI Gene 17345]
- **Chemicals:** oxypeucedanin (PubChem CID 33306), temozolomide (PubChem CID 5394)
- **Diseases:** Glioblastoma multiforme (MONDO:0018177), GBM (MONDO:0018177)

## Full-text entities

- **Genes:** BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}
- **Diseases:** GBM (MESH:D005909), brain tumor (MESH:D001932)
- **Chemicals:** TMZ (MESH:D000077204), MTT (MESH:C070243), trypan blue (MESH:D014343), OP (MESH:C031535)

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12777718/full.md

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Source: https://tomesphere.com/paper/PMC12777718