CD133 prevents colon cancer cell death induced by serum deprivation through activation of Akt‐mediated protein synthesis and inhibition of apoptosis. Issue 5 (28th March 2021)

• Record Type: Journal Article
• Authors: Mori, Yusuke; Takeuchi, Ayaka; Miyagawa, Kengo; Yoda, Hiroyuki; Soda, Hiroaki; Nabeya, Yoshihiro; Watanabe, Naoko; Ozaki, Toshinori; Shimozato, Osamu
• Editors: Kobarg, Jörg
• Is Part Of: FEBS open bio. Volume 11:Issue 5(2021)
• Page Start: 1382
• Page End: 1394
• Publication Date: 2021-03-28
• Subjects: Akt -- CD133 -- colon carcinoma -- resistance to nutritional stress; Molecular biology -- Periodicals; Cytology -- Periodicals; Life sciences -- Periodicals; Biological Science Disciplines -- Periodicals; Molecular Biology -- Periodicals; Cell Biology -- Periodicals; Cytology; Life sciences; Molecular biology; Periodicals; 572.805
• DOI: 10.1002/2211-5463.13145
• Languages: English
• ISSNs: 2211-5463

Abstract

Abstract : During the early phase of tumorigenesis, primary malignant cells survive within a low nutrition environment caused by a poorly organized vascular system. Here, we sought to determine the functional significance of CD133 in the survival of cancer cells under nutrient‐poor conditions. Knockdown and overexpression experiments demonstrated that CD133 suppresses colon cancer cell death induced by serum deprivation through activation of Akt‐mediated anti‐apoptosis and protein synthesis pathways. Furthermore, serum deprivation increased the amount of endogenous CD133 protein, which was regulated at least in part by phosphoinositide 3‐kinase. Thus, it is highly likely that CD133 contributes to the acquisition/maintenance of the resistance to stress arising from nutrient deficiency in early avascular tumor tissues. Abstract : During tumorigenesis, primary malignant cells survive within a low nutrition environment as a result of a poorly organized vascular system. Here, we investigated the significance of CD133 in the survival of cancer cells under nutrient‐poor conditions. Our results suggest that CD133 contributes to the growth of tumors, in which nutrients are poorly supplied, through Akt‐mediated anti‐apoptosis and protein synthesis pathways.