Open Access<p>Foretinib Inhibits Cancer Stemness and Gastric Cancer Cell Proliferation by Decreasing CD44 and c-MET Signaling</p>
Author(s) -
Sung-Hwa Sohn,
Bohyun Kim,
Hee Jung Sul,
Bo Youn Choi,
Hyeong Su Kim,
Dae Young Zang
Publication year - 2020
Publication title -
oncotargets and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.054
H-Index - 60
ISSN - 1178-6930
DOI - 10.2147/ott.s226951
Subject(s) - cd44 , cancer research , receptor tyrosine kinase , c met , protein kinase b , cell growth , cancer cell , flow cytometry , apoptosis , cancer , chemistry , biology , microbiology and biotechnology , cell , signal transduction , medicine , receptor , biochemistry , hepatocyte growth factor
CD44 isoforms are highly expressed in cancer stem cells, initiating tumor growth and sustaining tumor self-renewal. Among these isoforms, CD44 variant 9 (CD44v9) is overexpressed in chronic inflammation-induced cancer. CD44 and the mesenchymal-to-epithelial transition (MET) receptor tyrosine kinase are coactivated in some gastric cancers (GCs). In this study, we characterized MET and CD44 expression and signaling in human GC cell lines and analyzed differences in the susceptibility of these lines to foretinib.