Using an in vitro model of carcinogenesis we aimed at experimentally elucidating the significance of heterogeneity in the expression of CD24, a marker frequently overexpressed in various cancers and correlated with poor prognosis.
These observations identify AQP3 and CD24 as biomarkers for carcinogenesis of GIM, and may provide a precise strategy for screening at-risk candidates with GIM.
Striving for an integrated view of the intracellular signaling processes involved, we discuss the most pertinent routes of CD24-mediated signaling pathways and functional networks in neurobiology (neural migration, neurite extension, neurogenesis) and pathology (tumorigenesis, multiple sclerosis).
To clarify the possible roles of epithelial cell adhesion molecule (TROP-1/Ep-CAM) and CD24 molecule (CD24) in ovarian tumorigenesis, and explore the possible mechanism underlying this disease.
CD24 is shown in vitro and in vivo as being an important oncogene in the gut, and one that plays a critical role in the initiation and progression of carcinogenesis.
Taken together, our results indicate that CD24 mediates gastric carcinogenesis and may promote GC progression by suppressing apoptosis and promoting invasion, with the activation of STAT3 playing a critical role.
Study in xenografted mice further showed that CD24(-)CD44(+)Grp78(+) cells exhibited highest tumorigenesis, compared with CD24(-)CD44(+) CD24(+)CD44(+) or the parental cells.
As a small heavily glycosylated mucin-like glycosyl-phosphatidylinositol-anchored cell surface protein, CD24 plays an important role in carcinogenesis of various human malignancies.
Compared with HER2-negative BCSCs, HER2(+)/CD44(+)/CD24(-/low) cells showed elevated aldehyde dehydrogenase (ALDH) activity and aggressiveness tested by Matrigel invasion, tumor sphere formation, and in vivo tumorigenesis.
It also leads to features associated with breast-cancer-initiating cells: increased CD24(low)-CD44(high) population of cells, mammosphere formation and tumorigenesis.