INTERNATIONAL CONGRESS OF
CancerGenetics
Sialic Acid Attenuates Temozolomide-Induced Apoptosis in 1321N1 Glioma Cells via Downregulation of BAX Expression
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Farideh Rezaei,1,* Mohammad Shafiei,2 Hamid Galehdari,3 Alireza Malayeri,4 Seyed Mehdi Kalantar,5
1. Department of Biology, Faculty of Science, Golestan University, Gorgan, Iran
2. Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
3. Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
4. Medical Plant Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
5. Research and Clinical Center for Infertility, Shahid Sadoughi Medical Sciences University, Yazd, Iran.
- Introduction: Failure of apoptosis is a defining feature of glioma and a major barrier to effective chemotherapy. Although temozolomide (TMZ) remains the backbone of glioma treatment, its clinical benefit is frequently undermined by resistance mechanisms shaped by the tumor microenvironment. Among these, sialic acid has emerged as a potential regulator of malignant cell survival, yet its influence on apoptosis-related genes in glioma remains poorly understood. This study examined whether sialic acid alters BAX expression and interferes with TMZ-driven apoptotic signaling.
- Methods: Human 1321N1 glioma cells were exposed to TMZ (215 and 100 µM), sialic acid (500 and 300 µM), or their combination for 48 and 72 hours. Following treatment, BAX transcript levels were quantified using qRT-PCR to evaluate treatment-associated changes in apoptotic gene regulation.
- Results: TMZ exposure increased BAX expression, consistent with activation of a pro-apoptotic response. In contrast, sialic acid reduced BAX levels, indicating suppression of apoptosis-related signaling. More importantly, the combination of TMZ with sialic acid diminished BAX expression relative to TMZ treatment alone, suggesting that sialic acid may blunt the apoptotic pressure exerted by chemotherapy. These findings support a model in which sialic acid shifts glioma cells toward a more therapy-tolerant state.
- Conclusion: Our data identify sialic acid as a potential modulator of apoptotic susceptibility in glioma cells. By attenuating BAX expression, sialic acid may limit the effectiveness of TMZ and promote a chemoresistant phenotype. Targeting sialylation-associated pathways could therefore represent a mechanistically relevant strategy for restoring apoptosis and improving glioma treatment response.
- Keywords: Glioma Apoptosis BAX Gene Expression Sialylation Temozolomide Resistance
