It was also demonstrated that ICG‑001 downregulated the expression of CD44, and this effect was accompanied by restored expression of microRNA (miRNA)‑150 in various NPC cell lines.
Moreover, our results demonstrated that miR-328 suppressed NPC cell migration and inhibited the epithelial-mesenchymal transition process directly through a binding site on the CD44 3' untranslated region.
Our previous study reported that Epstein-Barr virus(EBV)-encoded latent membrane protein 1 (LMP1) could induce development of CD44(+/High) stem-like cells in nasopharyngeal carcinoma (NPC).
Notably, the proliferation, colony formation, migration, and invasion capabilities of the sequence-specific short hairpin RNA lentivirus-infected CD44(+) nasopharyngeal carcinoma cells reduced significantly under chemotherapeutic treatments (P < .05).
Germline variants in CD44 gene have been associated with susceptibility to breast and nasopharyngeal carcinomas but no study in gallbladder cancer (GBC) has been done yet.
Treatment with anti-CD44 antibodies in NPC parental cells not only resulted in a decrease of FLJ10540 protein, but also affected the abilities of FLJ10540-elicited cell growth and motility in osteopontin stimulated-NPC cells.
Our results showed that (a) platelet-NPC aggregates (PNA) were associated with higher shear-induced P-selectin expression and glycoprotein alpha(II)beta(3) activation than platelet-platelet aggregates (PPA); (b) strenuous exercise (SE, up to VO2max), but not moderate exercise (ME, 60% VO2max for 30 min), increased both PPA and PNA in mimicked venous and arterial circuits and enhanced PNA in mimicked flow of stenotic vessels; (c) the percentages of PNA that remained bound to ECs in mimicked flow of post-capillary venules increased, while platelet-induced CD44 cleavage on NPC and trans-endothelial migration of NPC were enhanced following SE, but were unchanged in response to ME.