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Calcium signaling induces a partial EMT.

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机构： [1]Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA. [2]Department of Internal Medicine and Children's Research Institute, UT Southwestern Medical Center, Dallas, TX, USA. [3]Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA, USA. [4]Department of Biochemistry and Molecular Biophysics, University of Pennsylvania, Philadelphia, PA, USA. [5]Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. [6]Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA. [7]Moores Cancer Center, University of California, San Diego, La Jolla, CA, USA. [8]State Key Laboratory of Oral Diseases, National Clinical Research for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu, China. [9]Children's Cancer and Blood Foundation Laboratories, Departments of Pediatrics, and Cell and Developmental Biology, Drukier Institute for Children's Health, Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA. [10]Centre for BioSystems Science and Engineering, Indian Institute of Science, Bangalore, India. [11]Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. [12]Division of Digestive and Liver Diseases, Department of Medicine, Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, USA.

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关键词： calcium cellular plasticity E-cadherin partial EMT

摘要：

Epithelial plasticity, or epithelial-to-mesenchymal transition (EMT), is a well-recognized form of cellular plasticity, which endows tumor cells with invasive properties and alters their sensitivity to various agents, thus representing a major challenge to cancer therapy. It is increasingly accepted that carcinoma cells exist along a continuum of hybrid epithelial-mesenchymal (E-M) states and that cells exhibiting such partial EMT (P-EMT) states have greater metastatic competence than those characterized by either extreme (E or M). We described recently a P-EMT program operating in vivo by which carcinoma cells lose their epithelial state through post-translational programs. Here, we investigate the underlying mechanisms and report that prolonged calcium signaling induces a P-EMT characterized by the internalization of membrane-associated E-cadherin (ECAD) and other epithelial proteins as well as an increase in cellular migration and invasion. Signaling through Gαq-associated G-protein-coupled receptors (GPCRs) recapitulates these effects, which operate through the downstream activation of calmodulin-Camk2b signaling. These results implicate calcium signaling as a trigger for the acquisition of hybrid/partial epithelial-mesenchymal states in carcinoma cells.© 2021 The Authors.

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出版当年[2021]版：

大类 | 1 区

生物学

小类 | 2 区生化与分子生物学 2 区细胞生物学

最新[2023]版：

大类 | 1 区

生物学

小类 | 2 区生化与分子生物学 2 区细胞生物学

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第一作者机构： [1]Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

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通讯机构： [1]Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA. [11]Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

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Calcium signaling induces a partial EMT.

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