Name: URI alleviates tyrosine kinase inhibitors-induced ferroptosis by reprogramming lipid metabolism in p53 wild-type liver cancers. HEK293T cells were transfected with His-URI plasmid before anti-His immunoprecipitation and gel cutting. LC-MS/MS was performed to identify URI potential binding proteins.
Keywords: Uri

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URI alleviates tyrosine kinase inhibitors-induced ferroptosis by reprogramming lipid metabolism in p53 wild-type liver cancers. HEK293T cells were transfected with His-URI plasmid before anti-His immunoprecipitation and gel cutting. LC-MS/MS was performed to identify URI potential binding proteins.

ABSTRACT: URI keeps low levels of p53 in a TRIM28-MDM2 dependent manner, maintains SCD1 activity and accumulation of MUFAs, and subsequently promotes resistance to TKIs in cancer cell. URI-p53-SCD1 axis mediates resistance of TKIs and may explain why p53-wild type HCC still showed intrinsic resistance to TKIs. Moreover, the combination therapy identified here may represent a promising strategy for the approximately 41% of patients with advanced HCC who have wild-type p53 and high levels of URI/SCD1.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Early Embryonic Cell

DISEASE(S): Disease Free

SUBMITTER: Zhiwen Ding

LAB HEAD: Liwei Dong

PROVIDER: PXD045407 | Pride | 2023-09-15

REPOSITORIES: Pride

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