ArticleMolecular cancer2020
β-catenin represses miR455-3p to stimulate m6A modification of HSF1 mRNA and promote its translation in colorectal cancer.
Article in Molecular cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed.
- Identification of super-enhancer-based biomarkers for predicting survival and immunotherapy efficacy in colorectal cancer.Journal of Cancer · 2026Article
- Crosstalk between mFrontiers in immunology · 2026Review
- METTL3 in colorectal cancer: molecular insights and clinical implications.Molecular biology reports · 2025Review
- Pan-cancer analysis reveals the prognostic and immunomodulatory potential of super-enhancer-induced ANGPT2 and experimental validation in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C-Myc Feedback Loop.MedComm · 2025Article
- Integrative analysis reveals therapeutic potential of pyrvinium pamoate in Merkel cell carcinoma.The Journal of clinical investigation · 2025Article
- IL-33 aggravates extranodal NK/T cell lymphoma aggressiveness and angiogenesis by activating the Wnt/β-catenin signaling pathway.Molecular and cellular biochemistry · 2025Article
- POLE2 silencing inhibits the progression of colorectal carcinoma cells via wnt signaling axis.Cancer biology & therapy · 2024Article
- Integrative analysis reveals therapeutic potential of pyrvinium pamoate in Merkel cell carcinoma.bioRxiv : the preprint server for biology · 2024Article
- Overview of the interplay between m6A methylation modification and non-coding RNA and their impact on tumor cells.Translational cancer research · 2024Review
- The m6A Reader YTHDC2 Suppresses Lung Adenocarcinoma Tumorigenesis by Destabilizing MRPL12.Molecular biotechnology · 2024Article
- Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024Review
- Protein translation: biological processes and therapeutic strategies for human diseases.Signal transduction and targeted therapy · 2024Review
- Link between m6A modification and infiltration characterization of tumor microenvironment in lung adenocarcinoma.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Heat Shock Factor 1 Inhibition: A Novel Anti-Cancer Strategy with Promise for Precision Oncology.Cancers · 2023Review
- Clostridium butyricum inhibits epithelial-mesenchymal transition of intestinal carcinogenesis through downregulating METTL3.Cancer science · 2023Article
- Prognostic value of comprehensive typing based on m6A and gene cluster in TNBC.Journal of cancer research and clinical oncology · 2023Article
- Identification of osteosarcoma m6A-related prognostic biomarkers using artificial intelligence: RBM15.Scientific reports · 2023Article
- The landscape of meLife · 2023Article
- RNA mMolecular oncology · 2023Review
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12 authors.
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Abstract
backgroundHeat 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.
methodsHSF1 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 APC
resultsHSF1 expression and activity were reduced after the inhibition of WNT/β-catenin signaling by pyrvinium or β-catenin knockdown, but elevated upon its activation by lithium chloride (LiCl) or β-catenin overexpression. There are much less upregulated genes in HSF1-KO MEF treated with LiCl when compared with LiCl-treated WT MEF. HSF1 protein expression was positively correlated with β-catenin expression in cell lines and primary tissues. After β-catenin depletion, HSF1 mRNA translation was impaired, accompanied by the reduction of its m6A modification and the upregulation of miR455-3p, which can interact with 3'-UTR of HSF1 mRNA to repress its translation. Interestingly, inhibition of miR455-3p rescued β-catenin depletion-induced reduction of HSF1 m6A modification and METTL3 interaction. Both the size and number of tumors were significantly reduced in APC
conclusionsβ-catenin suppresses miR455-3p generation to stimulate m6A modification and subsequent translation of HSF1 mRNA. HSF1 is important for β-catenin to promote CRC development. Targeting HSF1 could be a potential strategy for the intervention of β-catenin-driven cancers.
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