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10.1007/s00018-022-04417-9

http://scihub22266oqcxt.onion/10.1007/s00018-022-04417-9
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35773608!10428948!35773608
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suck abstract from ncbi

pmid35773608      Cell+Mol+Life+Sci 2022 ; 79 (7): 389
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  • EWI2 prevents EGFR from clustering and endocytosis to reduce tumor cell movement and proliferation #MMPMID35773608
  • Fu C; Wang J; Pallikkuth S; Ding Y; Chen J; Wren JD; Yang Y; Wong KK; Kameyama H; Jayaraman M; Munshi A; Tanaka T; Lidke KA; Zhang XA
  • Cell Mol Life Sci 2022[Jun]; 79 (7): 389 PMID35773608show ga
  • EWI2 is a transmembrane immunoglobulin superfamily (IgSF) protein that physically associates with tetraspanins and integrins. It inhibits cancer cells by influencing the interactions among membrane molecules including the tetraspanins and integrins. The present study revealed that, upon EWI2 silencing or ablation, the elevated movement and proliferation of cancer cells in vitro and increased cancer metastatic potential and malignancy in vivo are associated with (i) increases in clustering, endocytosis, and then activation of EGFR and (ii) enhancement of Erk MAP kinase signaling. These changes in signaling make cancer cells (i) undergo partial epithelial-to-mesenchymal (EMT) for more tumor progression and (ii) proliferate faster for better tumor formation. Inhibition of EGFR or Erk kinase can abrogate the cancer cell phenotypes resulting from EWI2 removal. Thus, to inhibit cancer cells, EWI2 prevents EGFR from clustering and endocytosis to restrain its activation and signaling.
  • |*Antigens, CD/metabolism[MESH]
  • |*Endocytosis[MESH]
  • |*ErbB Receptors/genetics/metabolism[MESH]
  • |*Membrane Proteins/deficiency/genetics/metabolism[MESH]
  • |*Neoplasms/genetics/metabolism/pathology[MESH]
  • |Cell Line, Tumor[MESH]
  • |Cell Movement/physiology[MESH]
  • |Cell Proliferation/physiology[MESH]
  • |Epithelial-Mesenchymal Transition[MESH]
  • |Humans[MESH]


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