Molecular Regulation of Autophagy and Asymmetric Cell Division by Cancer Stem Cell Marker CD133

CD133, also called prominin-1, is widely known as a cancer stem cell marker, and its high expression correlates with a poor prognosis in many cancers. CD133 was originally discovered as a plasma membranous protein in stem/progenitor cells. It is now known that Src family kinases phosphorylate the C-terminal of CD133. However, when Src kinase activity is low, CD133 is not phosphorylated by Src and is preferentially downregulated into cells through endocytosis. Endosomal CD133 then associates with HDAC6, thereby recruiting it to the centrosome via dynein motors. Thus, CD133 protein is now known to localize to the centrosome as endosomes as well as to the plasma membrane. More recently, a mechanism to explain the involvement of CD133 endosomes in asymmetric cell division was reported. Here, we would like to introduce the relationship between autophagy regulation and asymmetric cell division mediated by CD133 endosomes.

Automated summary

CD133, also known as prominin-1, is a well-known cancer stem cell marker associated with poor prognosis in many cancers. It was originally identified as a plasma membranous protein in stem/progenitor cells and is phosphorylated by Src family kinases. However, when Src kinase activity is low, CD133 is downregulated through endocytosis and associates with HDAC6, allowing it to localize to the centrosome. Recent studies have also revealed the involvement of CD133 endosomes in asymmetric cell division, providing insights into the regulation of autophagy.