2. Academic Validation
  3. Par3 promotes breast cancer invasion and migration through pull tension and protein nanoparticle-induced osmotic pressure

Par3 promotes breast cancer invasion and migration through pull tension and protein nanoparticle-induced osmotic pressure

  • Biomed Pharmacother. 2022 Sep 27;155:113739. doi: 10.1016/j.biopha.2022.113739.
Yunfeng Hu 1,  Qiu Xie 1,  Shanshan Chen 2,  Wangxing Zhao 1,  Xudong Zhao 3,  Qinli Ruan 1,  Zihui Zheng 1,  Huanhuan Zhao 1,  Tonghui Ma 1,  Jun Guo 4,  Lei Li 5
Affiliations

Affiliations

  • 1 School of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu, PR China.
  • 2 Department of Basic Medicine, Jiangsu College of Nursing, Huai'an 223005, Jiangsu, PR China.
  • 3 Department of General Practice, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, Jiangsu, PR China.
  • 4 School of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu, PR China. Electronic address: guoj@njucm.edu.cn.
  • 5 Department of General Practice, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221002, Jiangsu, PR China. Electronic address: ligroup-999@163.com.
PMID: 36179489 DOI: 10.1016/j.biopha.2022.113739
Abstract

Cancer cell invasion and metastasis are closely related to intracellular tension. The cell-polarity protein, Par3, is a mechanical transmitter that affects cytoskeletal forces and determines breast Cancer aggressiveness. Increased Par3 tension caused by aPKC inactivation is involved in filopodia and lamellipodia formation. Blocking the connection between Par3 and aPKC increases breast Cancer aggressiveness both in vitro and in vivo. Meanwhile, aPKC-induced Par3 cytoplasmic translocation results in JAM-A phase separation and microfilament depolymerization, which is associated with increased intracellular protein nanoparticle-induced osmotic pressure. This study demonstrated the effects of aPKC on Par3 tension and osmotic pressure in breast Cancer metastasis, and introduced Par3-associated mechanical mechanisms as potential targets for breast Cancer treatment.

Keywords

Breast cancer; FRET; Intracellular structural tension; Invasion; Par3; Protein nanoparticle.

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