FBXW7-mutated colorectal cancer cells exhibit aberrant expression of phosphorylated-p53 at Serine-15

摘要: FBXW7 mutations occur in a variety of human cancers including colorectal cancer (CRC). Elucidating its mechanism action has become crucial for therapy; however, it is also complicated by the fact that can influence many pathways due to role as an E3-ubiquitin ligase proteasome degradation. and TP53 are tumour suppressors intensively implicated carcinogenesis. Deletion these two genes animal models mark progression from adenoma carcinoma. Although still largely unknown, last defense against CRC at molecular level could be through synergistic effect genes. The underlying requires further investigation. In our laboratory, we have used phospho-kinase profiler array illustrate potential link between p53 cells. vitro vivo assessments demonstrated aberrant induction phosphorylated Serine 15 [phospho-p53(Ser15)] FBXW7-deficient cells compared their FBXW7-wild-type counterparts. loss HCT116 promoted resistance oxaliplatin. Immunoblotting data confirmed reduction phospho-p53(Ser15) may contribute decreased efficacy therapy FBXW7-mutated findings suggest applicability indicative marker FBXW7-mutations. Phospho-p53(Ser15) regulation E3-ligase activity provide important clues understanding behavior grounds clinical thereafter.