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作 者:Haokun Yuan Ruiqin Fang Chi Fu Shuo Wang Xiaoqin Tong Deyi Feng Xiaoqing Wei Xirong Hu Yuan Wang
机构地区:[1]The Key Laboratory for Human Disease Gene Study of Sichuan Province and the Department of Laboratory Medicine,Sichuan Provincial People's Hospital,School of Medicine,University of Electronic Science and Technology of China,Chengdu 610072,China [2]The School of Medicine,University of Electronic Science and Technology of China,Chengdu 610054,China [3]The School of Life Science,University of Electronic Science and Technology of China,Chengdu 610054,China [4]State Key Laboratory of Cellular Stress Biology,School of Life Sciences,Xiamen University,Xiamen 361104,China
出 处:《Acta Biochimica et Biophysica Sinica》2024年第2期304-314,共11页生物化学与生物物理学报(英文版)
基 金:This work was supported by the grants from the Department of Science and Technology of Sichuan Province(Nos.2021ZYD0092 and 2022NSFSc0721);the Fundamental Research Funds for the Central Universities(Nos.ZYGX2021J024 and Y030222059002005).
摘 要: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 Il 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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