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<p>Epigenetic regulation plays a pivotal role in cancer progression and therapy. This study explores the therapeutic potential of siRNA-mediated CTLA-4 inhibition as an epigenetic intervention in esophageal cancer. The effects on cellular behavior and genetic pathways were assessed by suppressing <i>CTLA-4</i> expression in TE-8 esophageal cancer cells through targeted siRNA transfection. Cell viability, apoptosis, and cell cycle progression were evaluated using MTT assays, flow cytometry, and qRT-PCR. <i>CTLA-4</i> knockdown resulted in a marked reduction in cell viability, induction of apoptosis, and cell cycle arrest in the Sub-G1 phase. Gene expression analysis revealed significant upregulation of pro-apoptotic markers (<i>CASP-3</i>, <i>CASP-9</i>, <i>and BAX</i>) and downregulation of the anti-apoptotic gene <i>BCL-2</i>. These findings underscore the role of CTLA-4 in epigenetically modulating apoptotic pathways and suppressing tumor proliferation. This study highlights the potential of targeting CTLA-4 as an innovative epigenetic strategy in cancer treatment, providing insights into the intersection of genetics, epigenetics, and immunotherapy. By advancing our understanding of CTLA-4-related pathways, this research contributes to developing precision medicine approaches tailored to individual epigenetic profiles. Future studies should focus on in vivo validation and expanding these findings to other cancer models to promote equitable healthcare and personalized oncology solutions.</p>

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Epigenetic Modulation of CTLA-4 Via siRNA: A Novel Approach to Induce Apoptosis in TE-8 Esophageal Cancer Cells

  • 期刊论文

  • 发表日期：

    2025年11月27日

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  • Mahya Ahmadpour Youshanlui,
  • Sahand Eslami,
  • Amir Baghbanzadeh,
  • Mahdi Zarei,
  • Leili Aghebati Maleki

摘要

Epigenetic regulation plays a pivotal role in cancer progression and therapy. This study explores the therapeutic potential of siRNA-mediated CTLA-4 inhibition as an epigenetic intervention in esophageal cancer. The effects on cellular behavior and genetic pathways were assessed by suppressing CTLA-4 expression in TE-8 esophageal cancer cells through targeted siRNA transfection. Cell viability, apoptosis, and cell cycle progression were evaluated using MTT assays, flow cytometry, and qRT-PCR. CTLA-4 knockdown resulted in a marked reduction in cell viability, induction of apoptosis, and cell cycle arrest in the Sub-G1 phase. Gene expression analysis revealed significant upregulation of pro-apoptotic markers (CASP-3, CASP-9, and BAX) and downregulation of the anti-apoptotic gene BCL-2. These findings underscore the role of CTLA-4 in epigenetically modulating apoptotic pathways and suppressing tumor proliferation. This study highlights the potential of targeting CTLA-4 as an innovative epigenetic strategy in cancer treatment, providing insights into the intersection of genetics, epigenetics, and immunotherapy. By advancing our understanding of CTLA-4-related pathways, this research contributes to developing precision medicine approaches tailored to individual epigenetic profiles. Future studies should focus on in vivo validation and expanding these findings to other cancer models to promote equitable healthcare and personalized oncology solutions.