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<p>Doxorubicin is an effective treatment for breast cancer, but drug resistance poses a significant challenge. Emerging regulators of drug resistance include microRNAs, small non-coding RNAs. Two miRNAs, miR-526b and miR-655, promote aggressive breast cancer phenotypes like cell proliferation, cancer stem cell upregulation, altered response to oxidative and metabolic stress and help tumor metastasis by activating COX-2/EP4/PI3K pathways. However, their impact on the effects of chemotherapeutic treatments remains unexplored. This study investigates the impact of overexpressing miR-526b and miR-655 on doxorubicin responses in breast cancer, focusing on pro-survival, apoptotic, and DNA-damage response pathways. We confirm the role of PI3K/Akt signalling in promoting cell survival and resistance in response to doxorubicin in vitro, though key differences exist between each cell line. High-throughput analysis of doxorubicin-exposed breast cancer cell lines, revealing novel mechanisms of miR-526b and miR-655. Overexpression of miR-526b and miR-655 may alter doxorubicin efficacy through mechanisms like DNA damage response changes, metabolic reprogramming, and immune pathway activation. Further investigation may uncover new therapeutic strategies to improve treatment efficacy and patient outcomes.</p>

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Investigating the effects of miR-526b and miR-655 on doxorubicin sensitivity in breast cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月29日

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  • Reid Morgan Opperman,
  • Sujit Maiti,
  • Mousumi Majumder

摘要

Doxorubicin is an effective treatment for breast cancer, but drug resistance poses a significant challenge. Emerging regulators of drug resistance include microRNAs, small non-coding RNAs. Two miRNAs, miR-526b and miR-655, promote aggressive breast cancer phenotypes like cell proliferation, cancer stem cell upregulation, altered response to oxidative and metabolic stress and help tumor metastasis by activating COX-2/EP4/PI3K pathways. However, their impact on the effects of chemotherapeutic treatments remains unexplored. This study investigates the impact of overexpressing miR-526b and miR-655 on doxorubicin responses in breast cancer, focusing on pro-survival, apoptotic, and DNA-damage response pathways. We confirm the role of PI3K/Akt signalling in promoting cell survival and resistance in response to doxorubicin in vitro, though key differences exist between each cell line. High-throughput analysis of doxorubicin-exposed breast cancer cell lines, revealing novel mechanisms of miR-526b and miR-655. Overexpression of miR-526b and miR-655 may alter doxorubicin efficacy through mechanisms like DNA damage response changes, metabolic reprogramming, and immune pathway activation. Further investigation may uncover new therapeutic strategies to improve treatment efficacy and patient outcomes.