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  • Investigating the Effect of Paclitaxel on BAX Gene Expression in MDA-MB-231 Breast Cancer Cell Line

  • Fatemeh Aghazadeh,1,* Seyed Jalal Zargar,2 Shahrokh Safarian,3
    1. Department of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran
    2. Department of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran
    3. Department of Cell and Molecular Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran


  • Introduction: Triple-Negative Breast Cancer (TNBC) is considered one of the most aggressive subtypes of breast cancer and has limited targeted therapeutic options due to the lack of hormonal receptors and HER2. Paclitaxel, as one of the main chemotherapeutic agents, reduces the survival of cancer cells by disrupting microtubule function and activating cell death pathways. The BAX gene, as a key pro-apoptotic gene of the BCL-2 family, plays a central role in the intrinsic apoptosis pathway by increasing mitochondrial membrane permeability and facilitating cytochrome c release. This study aimed to investigate the effect of paclitaxel on BAX gene expression in the MDA-MB-231 cell line.
  • Methods: MDA-MB-231 cells were treated with the IC50 concentration of paclitaxel (determined by MTT assay). After 72 hours, total cellular RNA was extracted, and cDNA was synthesized. BAX gene expression level was evaluated using Real-time PCR, with GAPDH as the reference gene, and expression changes were calculated using the 2^-ΔΔCT method.
  • Results: Treatment with paclitaxel significantly increased BAX gene expression. The relative expression level of BAX in the treated group was approximately 5-fold higher than in the control group (P < 0.001). This increase in expression indicates the activation of the pro-apoptotic pathway at the genetic level by paclitaxel.
  • Conclusion: The results indicate that paclitaxel can induce the intrinsic apoptosis pathway in MDA-MB-231 cells through a significant increase in BAX gene expression, which may be one of the main mechanisms of its antiproliferative effect. This finding emphasizes the importance of regulating BCL-2 family proteins in the response of TNBC cells to paclitaxel and can serve as a basis for future studies on treatment personalization and identifying predictive biomarkers of treatment response.
  • Keywords: Breast Cancer, MDA-MB-231, Paclitaxel, BAX, Apoptosis, Real-time PCR

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