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Background <p>Breast cancer remains a leading cause of cancer-related deaths among women. Despite advancements in treatment, drug resistance and tumor progression continue to present major challenges. CD39, an ecto-nucleotidase that regulates adenosine signaling, has been implicated in cancer progression and resistance to chemotherapy. This study investigates the role of CD39 in modulating the response of breast cancer cells to paclitaxel.</p> Methods <p>Human breast cancer cell lines (MDA-MB-231, MDA-MB-468, and SKBR-3) were cultured, and CD39 expression was assessed. CD39 knockdown was achieved using siRNA transfection. The effects of CD39 inhibition on paclitaxel sensitivity were evaluated through MTT assays, apoptosis assays, cell cycle analysis, and wound healing assays. Gene expression was analyzed by quantitative PCR.</p> Results <p>CD39 expression was highest in MDA-MB-231 cells selected for further experiments. CD39 knockdown significantly increased paclitaxel sensitivity, lowering the IC50 from 0.52&#xa0;µg/ml to 0.07&#xa0;µg/ml. The combination of CD39 siRNA and paclitaxel treatment induced a substantial increase in apoptosis (63.78% vs. 43.81% with paclitaxel alone) and promoted G2 cell cycle arrest. Additionally, cell migration was significantly reduced, which was associated with decreased expression of MMP-9.</p> Conclusion <p>Targeting CD39 using siRNA enhances paclitaxel efficacy by promoting apoptosis, disrupting the cell cycle, and inhibiting migration in breast cancer cells. These findings suggest that CD39 inhibition may be a promising therapeutic strategy to overcome drug resistance and improve breast cancer treatment outcomes.</p>

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Comprehensive Inhibition of Breast Cancer Progression Through CD39 Targeting and Paclitaxel: Modulating Cell Proliferation, Apoptosis, and Migration

  • 期刊论文

  • 发表日期：

    2026年3月14日

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  • Sahand Eslami,
  • Mahya Ahmadpour Youshanlui,
  • Amir Baghbanzadeh,
  • Fereshteh Jamali,
  • Behzad Baradaran

摘要

Background

Breast cancer remains a leading cause of cancer-related deaths among women. Despite advancements in treatment, drug resistance and tumor progression continue to present major challenges. CD39, an ecto-nucleotidase that regulates adenosine signaling, has been implicated in cancer progression and resistance to chemotherapy. This study investigates the role of CD39 in modulating the response of breast cancer cells to paclitaxel.

Methods

Human breast cancer cell lines (MDA-MB-231, MDA-MB-468, and SKBR-3) were cultured, and CD39 expression was assessed. CD39 knockdown was achieved using siRNA transfection. The effects of CD39 inhibition on paclitaxel sensitivity were evaluated through MTT assays, apoptosis assays, cell cycle analysis, and wound healing assays. Gene expression was analyzed by quantitative PCR.

Results

CD39 expression was highest in MDA-MB-231 cells selected for further experiments. CD39 knockdown significantly increased paclitaxel sensitivity, lowering the IC50 from 0.52 µg/ml to 0.07 µg/ml. The combination of CD39 siRNA and paclitaxel treatment induced a substantial increase in apoptosis (63.78% vs. 43.81% with paclitaxel alone) and promoted G2 cell cycle arrest. Additionally, cell migration was significantly reduced, which was associated with decreased expression of MMP-9.

Conclusion

Targeting CD39 using siRNA enhances paclitaxel efficacy by promoting apoptosis, disrupting the cell cycle, and inhibiting migration in breast cancer cells. These findings suggest that CD39 inhibition may be a promising therapeutic strategy to overcome drug resistance and improve breast cancer treatment outcomes.