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Background <p>Prostate cancer (PCa) is a common leading cause of death worldwide and is recognized as the second most frequently diagnosed cancer in the male population, making it a significant focus of long-term oncological research. The <i>HOXD13</i> gene, belonging to the <i>HOX</i> gene family, has been associated with various malignancies, including breast and colon cancer, and is associated with prognostic outcomes. However, its specific role in prostate cancer remains to be elucidated.</p> Methods <p>The correlation of <i>HOXD13</i> expression in PCa was analyzed by UALCAN database. qRT-PCR and western blot assays were employed to assess the expression levels of HOXD13 in several prostate cancer cell lines. Construct siRNA and overexpression plasmids for <i>HOXD13</i> and transfect them into cells. Western blot was used to assess the knockdown efficiency of HOXD13 in the cells. The influence of <i>HOXD13</i> expression on cell proliferation in PC-3&#xa0;M and C4-2 cells was assessed by EDU staining. The role of <i>HOXD13</i> in cell migration and invasion of prostate cancer cells was detected by wound healing and transwell assay. Western blot analysis was performed to examine apoptosis-related proteins (C-caspase3, Bax, and Bcl-2) in PC-3&#xa0;M cells. The co-immunoprecipitation (Co-IP) assay evaluates the interaction between MDM2 and p53.</p> Results <p>An examination of the data obtained from the UALCAN database reveals that <i>HOXD13</i> was significantly reduced in prostate cancer tissues and correlated with patient survival. In prostate cancer cell lines, notably PC-3M, <i>HOXD13</i> expression was markedly reduced. Knockdown of <i>HOXD13</i> promotes PC-3&#xa0;M and C4-2 cells proliferation, migration, and invasion. However, the elevated expression of <i>HOXD13</i> hampers PC-3&#xa0;M and C4-2 cells proliferation, migration, and invasion. Furthermore, knockdown of <i>HOXD13</i> in PC-3&#xa0;M cells resulted in decreased levels of apoptosis markers, including C-caspase-3 and Bax. Co-immunoprecipitation assays demonstrated that <i>HOXD13</i> depletion enhanced the association between MDM2 and p53.</p> Conclusion <p>HOXD13 was a critical regulator in the pathogenesis of prostate cancer, modulating the MDM2/p53 signaling pathway to promote apoptosis.</p>

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HOXD13 knockdown attenuates apoptosis in prostate cancer via the upregulation of MDM2/p53 signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月6日

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  • Yongliang Ma,
  • Pan Qi,
  • Zongtao Ren,
  • Rui Liu,
  • Shufei Wei,
  • Aili Zhang

摘要

Background

Prostate cancer (PCa) is a common leading cause of death worldwide and is recognized as the second most frequently diagnosed cancer in the male population, making it a significant focus of long-term oncological research. The HOXD13 gene, belonging to the HOX gene family, has been associated with various malignancies, including breast and colon cancer, and is associated with prognostic outcomes. However, its specific role in prostate cancer remains to be elucidated.

Methods

The correlation of HOXD13 expression in PCa was analyzed by UALCAN database. qRT-PCR and western blot assays were employed to assess the expression levels of HOXD13 in several prostate cancer cell lines. Construct siRNA and overexpression plasmids for HOXD13 and transfect them into cells. Western blot was used to assess the knockdown efficiency of HOXD13 in the cells. The influence of HOXD13 expression on cell proliferation in PC-3 M and C4-2 cells was assessed by EDU staining. The role of HOXD13 in cell migration and invasion of prostate cancer cells was detected by wound healing and transwell assay. Western blot analysis was performed to examine apoptosis-related proteins (C-caspase3, Bax, and Bcl-2) in PC-3 M cells. The co-immunoprecipitation (Co-IP) assay evaluates the interaction between MDM2 and p53.

Results

An examination of the data obtained from the UALCAN database reveals that HOXD13 was significantly reduced in prostate cancer tissues and correlated with patient survival. In prostate cancer cell lines, notably PC-3M, HOXD13 expression was markedly reduced. Knockdown of HOXD13 promotes PC-3 M and C4-2 cells proliferation, migration, and invasion. However, the elevated expression of HOXD13 hampers PC-3 M and C4-2 cells proliferation, migration, and invasion. Furthermore, knockdown of HOXD13 in PC-3 M cells resulted in decreased levels of apoptosis markers, including C-caspase-3 and Bax. Co-immunoprecipitation assays demonstrated that HOXD13 depletion enhanced the association between MDM2 and p53.

Conclusion

HOXD13 was a critical regulator in the pathogenesis of prostate cancer, modulating the MDM2/p53 signaling pathway to promote apoptosis.