1. Academic Validation
  2. The RGD motif is involved in CD97/ADGRE5-promoted cell adhesion and viability of HT1080 cells

The RGD motif is involved in CD97/ADGRE5-promoted cell adhesion and viability of HT1080 cells

  • Sci Rep. 2019 Feb 6;9(1):1517. doi: 10.1038/s41598-018-38045-w.
Wen-Ye Tjong 1 Hsi-Hsien Lin 2 3 4 5
Affiliations

Affiliations

  • 1 Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
  • 2 Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan. hhlin@mail.cgu.edu.tw.
  • 3 Department of Microbiology and Immunology, College of Medicine, Chang Gung University, Taoyuan, Taiwan. hhlin@mail.cgu.edu.tw.
  • 4 Department of Anatomic Pathology, Chang Gung Memorial Hospital-Linkou, Taoyuan, Taiwan. hhlin@mail.cgu.edu.tw.
  • 5 Chang Gung Immunology Consortium, Chang Gung Memorial Hospital-Linkou, Taoyuan, Taiwan. hhlin@mail.cgu.edu.tw.
Abstract

CD97/ADGRE5 is an adhesion G protein-coupled receptor (aGPCR) involved in tumor cell adhesion, migration, angiogenesis, and Apoptosis. CD97 has been shown previously to stimulate angiogenesis by interacting with integrins on endothelial cells via an Arginine-Glycine-Aspartic acid (RGD) motif. In this report, the role of the RGD motif in tumor cell adhesion and Apoptosis was investigated using a previously-established HT1080 cell-based system. We found that the RGD motif is critical in CD97-promoted cell adhesion, in part due to the up-regulation of αvβ5 and α2β1 integrins, and that CD97 mediates its anti-apoptotic effect in extrinsic Apoptosis via RGD-dependent cell adhesion. In contrast, CD97-modulated anti-apoptotic effect in intrinsic Apoptosis is mediated by RGD-independent, N-cadherin-induced homotypic cell aggregation. Hence, CD97 promotes tumorigenesis via RGD-dependent and -independent mechanisms.

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