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<p>Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with conventional therapies often limited by toxicity and resistance. Nanotechnology offers a novel approach by utilizing the unique properties of nanomaterials for targeted delivery. Beta-tricalcium phosphate (β-TCP), widely used in bone regeneration, has recently been explored for its anticancer potential. Its biocompatibility and nanoscale dimensions allow it to effectively interfere with cellular signaling pathways, thereby targeting uncontrolled proliferation and apoptosis evasion in cancer cells.The biological effects of β-TCP nanoparticles were examined on Calu-6 lung cancer and HEK-293 normal cells. Nanoparticles were synthesized and characterized using standard physicochemical techniques, and their biological effects were assessed through cell viability (MTT assay), nuclear morphology (DAPI staining), and apoptosis/necrosis analysis (Annexin V-FITC/PI flow cytometry). The expression of key genes (p53, Caspase-3, and Caspase-9) was quantified using RT-qPCR. The synthesized β-TCP nanoparticles demonstrated favorable properties, including colloidal stability, nanoscale morphology, and phase purity. The nanoparticles induced a dose-dependent reduction in the viability of Calu-6 cells, while normal HEK-293 cells showed a high level of viability, indicating a selective cytotoxic effect. Analysis of cell death mechanisms confirmed that apoptosis was the dominant pathway. Furthermore, quantitative gene expression analysis revealed a significant, concentration-dependent upregulation of key pro-apoptotic genes, specifically tumor protein p53, Caspase-9, and Caspase-3, thereby confirming the activation of the intrinsic apoptotic pathway. β-TCP nanoparticles exhibit strong anti-proliferative and pro-apoptotic effects on Calu-6 lung cancer cells, primarily via the intrinsic apoptotic pathway, underscoring their therapeutic potential in lung cancer.</p>

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β-Tricalcium Phosphate Nanoparticles: A Novel Therapeutic Strategy Against Lung Carcinoma Through Apoptosis Induction and Proliferation Suppression in Calu-6 Cells via Intrinsic Signaling

  • 期刊论文

  • 发表日期：

    2025年9月27日

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  • Mohammadreza Pourmohammad,
  • Homa Mahmoudzadeh,
  • Navid Naderi Kalali,
  • Saeedeh Zafar Balanjad

摘要

Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with conventional therapies often limited by toxicity and resistance. Nanotechnology offers a novel approach by utilizing the unique properties of nanomaterials for targeted delivery. Beta-tricalcium phosphate (β-TCP), widely used in bone regeneration, has recently been explored for its anticancer potential. Its biocompatibility and nanoscale dimensions allow it to effectively interfere with cellular signaling pathways, thereby targeting uncontrolled proliferation and apoptosis evasion in cancer cells.The biological effects of β-TCP nanoparticles were examined on Calu-6 lung cancer and HEK-293 normal cells. Nanoparticles were synthesized and characterized using standard physicochemical techniques, and their biological effects were assessed through cell viability (MTT assay), nuclear morphology (DAPI staining), and apoptosis/necrosis analysis (Annexin V-FITC/PI flow cytometry). The expression of key genes (p53, Caspase-3, and Caspase-9) was quantified using RT-qPCR. The synthesized β-TCP nanoparticles demonstrated favorable properties, including colloidal stability, nanoscale morphology, and phase purity. The nanoparticles induced a dose-dependent reduction in the viability of Calu-6 cells, while normal HEK-293 cells showed a high level of viability, indicating a selective cytotoxic effect. Analysis of cell death mechanisms confirmed that apoptosis was the dominant pathway. Furthermore, quantitative gene expression analysis revealed a significant, concentration-dependent upregulation of key pro-apoptotic genes, specifically tumor protein p53, Caspase-9, and Caspase-3, thereby confirming the activation of the intrinsic apoptotic pathway. β-TCP nanoparticles exhibit strong anti-proliferative and pro-apoptotic effects on Calu-6 lung cancer cells, primarily via the intrinsic apoptotic pathway, underscoring their therapeutic potential in lung cancer.