Ontology highlight
ABSTRACT: Background
Heat shock transcription factor1 (HSF1) was overexpressed to promote glutaminolysis and activate mTOR in colorectal cancer (CRC). Here, we investigated the mechanism for cancer-specific overexpression of HSF1.Methods
HSF1 expression was analyzed by chromatin immunoprecipitation, qRT-PCR, immunohistochemistry staining and immunoblotting. HSF1 translation was explored by polysome profiling and nascent protein analysis. Biotin pulldown and m6A RNA immunoprecipitation were applied to investigate RNA/RNA interaction and m6A modification. The relevance of HSF1 to CRC was analyzed in APCmin/+ and APCmin/+ HSF1+/-mice.Results
HSF1 expression and activity were reduced after the inhibition of WNT/β-catenin signaling by pyrvinium or
SUBMITTER: Song P
PROVIDER: S-EPMC7446108 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature