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Background <p>Bladder cancer (BC) remains the leading global mortality and poor prognosis in genitourinary malignancies, especially in patients with metastasis.</p> Results <p>In this study, we demonstrate that loss of polarity protein partitioning defective 3 (Par3, encoded by <i>PARD3</i>) is correlated with stronger metastatic capability and a poorer prognosis in BC. Par3 deletion in high grade BC cells accelerates their invasion and metastasis in vitro and in vivo. Mechanistically, Par3 could directly interact with protein phosphatase 1 regulatory subunit 12&#xa0;C (Ppp1r12c). Either Par3 or Ppp1r12c over-expression rescues the invasion and metastasis caused by Par3 deficiency in vitro. Moreover, the actin filament-related processions are enriched in the downstream biological function, resulting from the activation of ERK 1/2 and p38 signaling pathways, indicated by proteomics analysis from BC cells and tissue, as well as data mining results from BC public database.</p> Conclusion <p>Together, our study reveals that Par3 deficiency promotes BC metastasis. Par3 directly interacts with Ppp1r12c (390-782aa), activating the Par3/Ppp1r12c/ERK/p38 axis. Par3 could act as a prognostic biomarker and potential therapeutic target for BC.</p>

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Polarity protein Par3 deficiency promotes metastasis of bladder cancer via interaction of Ppp1r12c

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Jinming Cai,
  • Can Jiao,
  • Yingying Xu,
  • Fang Zhang,
  • Li Zhang,
  • She Chen,
  • Bing Shen

摘要

Background

Bladder cancer (BC) remains the leading global mortality and poor prognosis in genitourinary malignancies, especially in patients with metastasis.

Results

In this study, we demonstrate that loss of polarity protein partitioning defective 3 (Par3, encoded by PARD3) is correlated with stronger metastatic capability and a poorer prognosis in BC. Par3 deletion in high grade BC cells accelerates their invasion and metastasis in vitro and in vivo. Mechanistically, Par3 could directly interact with protein phosphatase 1 regulatory subunit 12 C (Ppp1r12c). Either Par3 or Ppp1r12c over-expression rescues the invasion and metastasis caused by Par3 deficiency in vitro. Moreover, the actin filament-related processions are enriched in the downstream biological function, resulting from the activation of ERK 1/2 and p38 signaling pathways, indicated by proteomics analysis from BC cells and tissue, as well as data mining results from BC public database.

Conclusion

Together, our study reveals that Par3 deficiency promotes BC metastasis. Par3 directly interacts with Ppp1r12c (390-782aa), activating the Par3/Ppp1r12c/ERK/p38 axis. Par3 could act as a prognostic biomarker and potential therapeutic target for BC.