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<p>Previous studies have indicated that miR-592 may play a significant role in the development of various cancers, particularly in the proliferation and growth of breast cancer (BC) cells. However, the regulatory mechanism by which miR-592 influences apoptosis in BC cells remains unclear. In this study, functional assays investigating the role of miR-592 in apoptosis of MCF-7 cells were conducted, alongside transcriptome analysis using RNA-seq.&#xa0;The results demonstrate that miR-592 not only inhibits breast cancer progression but also promotes apoptosis in breast cancer cells. Several significantly dysregulated genes and enriched pathways were identified in response to miR-592 overexpression in MCF-7 cells. Among these, CYP20A1 was validated as a key target gene of miR-592, with its expression being negatively regulated by miR-592. Restoration of CYP20A1 expression reversed the pro-apoptotic and tumor-suppressive effects of miR-592 in MCF-7 cells. This process was mediated through activation of the C/EBP homologous protein (CHOP)-dependent endoplasmic reticulum stress-induced apoptotic pathway. Collectively, these findings indicate that CYP20A1 is involved in the regulation of the CHOP-mediated endoplasmic reticulum apoptosis pathway in miR-592-induced apoptosis in breast cancer cells.</p>

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MicroRNA-592 suppresses breast cancer progression by targeting CYP20A1 to modulate the CHOP pathway

  • 期刊论文

  • 发表日期：

    2025年10月15日

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  • Ruolan Pan,
  • Shangquan Jiang,
  • Jinxing Su,
  • Caiyun Zhang,
  • Xiaoxing Li,
  • Kan He

摘要

Previous studies have indicated that miR-592 may play a significant role in the development of various cancers, particularly in the proliferation and growth of breast cancer (BC) cells. However, the regulatory mechanism by which miR-592 influences apoptosis in BC cells remains unclear. In this study, functional assays investigating the role of miR-592 in apoptosis of MCF-7 cells were conducted, alongside transcriptome analysis using RNA-seq. The results demonstrate that miR-592 not only inhibits breast cancer progression but also promotes apoptosis in breast cancer cells. Several significantly dysregulated genes and enriched pathways were identified in response to miR-592 overexpression in MCF-7 cells. Among these, CYP20A1 was validated as a key target gene of miR-592, with its expression being negatively regulated by miR-592. Restoration of CYP20A1 expression reversed the pro-apoptotic and tumor-suppressive effects of miR-592 in MCF-7 cells. This process was mediated through activation of the C/EBP homologous protein (CHOP)-dependent endoplasmic reticulum stress-induced apoptotic pathway. Collectively, these findings indicate that CYP20A1 is involved in the regulation of the CHOP-mediated endoplasmic reticulum apoptosis pathway in miR-592-induced apoptosis in breast cancer cells.