Acta Biochimica et Biophysica Sinica (Jan 2024)

ATIP/ATIP1 regulates prostate cancer metastasis through mitochondrial dynamic-dependent signaling

  • Yuan Haokun,
  • Fang Ruiqin,
  • Fu Chi,
  • Wang Shuo,
  • Tong Xiaoqin,
  • Feng Deyi,
  • Wei Xiaoqing,
  • Hu Xirong,
  • Wang Yuan

DOI
https://doi.org/10.3724/abbs.2024006
Journal volume & issue
Vol. 56
pp. 304 – 314

Abstract

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Mitochondria play a fundamental role in cell survival and motility. Abnormalities in mitochondria are associated with carcinogenesis, especially with tumor metastasis. In this study, we explore the biological function of ATIP1, which is a mitochondrial-located isoform of angiotensin II AT2 receptor interacting proteins (ATIPs) in prostate cancer cells. The results showed that ATIP is downregulated in prostate cancer tissues and is negatively correlated with the disease-free survival rate of prostate cancer patients. Silencing of ATIP promotes mitochondrial fission and enhances tumor cell migration and invasion. Reconstitution of ATIP1 in ATIP-deficient cells significantly attenuates mitochondrial trafficking and tumor cell movement. Therefore, ATIP1 is a negative regulator of mitochondrial dynamics and tumor cell motility and is also a potential biomarker for predicting prostate cancer malignancy.

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