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Background <p>One of the crucial steps in the development of tumor metastasis is tumor cell invasion. This stage initiates a sequence of molecular interactions that enable invasive cells to adhere to the extracellular matrix (ECM) through the activity of cell adhesion molecules (CAMs). The primary cell surface receptor for ECM components is CD44. High levels of CD44 are necessary for breast cancer stem cells (BCSCs) to retain the multipotency of the BCSC population.</p> Aim <p>This study examines methods for focusing on tumour cells that overexpress CD44 and provides a thorough summary of CD44’s function in the development of breast cancer.</p> Methods <p>Using in vitro models, we evaluated the therapeutic potential of Adapalene, a repurposed drug that is often used to treat acne. Western blotting analysis was used to check the expression of resistance markers in Paclitaxel-resistant cells. The ability of Adapalene to target and exhibit CD44 expression was examined using immunocytochemistry methods. Additionally, we used an in <Emphasis Type="BoldItalic">silico</Emphasis>/docking technique to assess Adapalene’s interaction with CD44.</p> Results <p>According to our findings, Adapalene selectively kills TNBC cells rather than non-TNBC cells, particularly in the 4T1 model. Interestingly, drug-resistant produced MDA-MB-231 cells exhibited a 298-fold increase in ic50 value in comparison to the parental MDA-MB-231 cells. The findings showed that Adapalene targets CD44, a crucial stemness biomarker, to decrease the stemness traits of drug-resistant cells.</p> Conclusion <p>Overall, this study highlights how CD44 overexpression accelerates the growth of breast cancer and transforms drug-resistant cells into stem cells, and that targeting CD44 with Adapalene may significantly enhance therapy results and defer the onset of drug resistance in breast cancer patients.</p>

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Adapalene inhibits the activity of CD44, a cancer stem cell biomarker in Triple negative breast cancer

  • 期刊论文

  • 发表日期：

    2026年7月3日

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  • Shazia Sofi,
  • Nusrat Jan,
  • Gowhar Masoodi,
  • Shariqa Jan,
  • Syed Nisar Ahmad,
  • Umar Mehraj,
  • Manzoor Ahmad Mir

摘要

Background

One of the crucial steps in the development of tumor metastasis is tumor cell invasion. This stage initiates a sequence of molecular interactions that enable invasive cells to adhere to the extracellular matrix (ECM) through the activity of cell adhesion molecules (CAMs). The primary cell surface receptor for ECM components is CD44. High levels of CD44 are necessary for breast cancer stem cells (BCSCs) to retain the multipotency of the BCSC population.

Aim

This study examines methods for focusing on tumour cells that overexpress CD44 and provides a thorough summary of CD44’s function in the development of breast cancer.

Methods

Using in vitro models, we evaluated the therapeutic potential of Adapalene, a repurposed drug that is often used to treat acne. Western blotting analysis was used to check the expression of resistance markers in Paclitaxel-resistant cells. The ability of Adapalene to target and exhibit CD44 expression was examined using immunocytochemistry methods. Additionally, we used an in silico/docking technique to assess Adapalene’s interaction with CD44.

Results

According to our findings, Adapalene selectively kills TNBC cells rather than non-TNBC cells, particularly in the 4T1 model. Interestingly, drug-resistant produced MDA-MB-231 cells exhibited a 298-fold increase in ic50 value in comparison to the parental MDA-MB-231 cells. The findings showed that Adapalene targets CD44, a crucial stemness biomarker, to decrease the stemness traits of drug-resistant cells.

Conclusion

Overall, this study highlights how CD44 overexpression accelerates the growth of breast cancer and transforms drug-resistant cells into stem cells, and that targeting CD44 with Adapalene may significantly enhance therapy results and defer the onset of drug resistance in breast cancer patients.