STAT3 activation of miR-21 and miR-181b-1 via PTEN and CYLD are part of the epigenetic switch linking inflammation to cancer

Clicks: 264
ID: 270183
2010
A transient inflammatory signal can initiate an epigenetic switch from nontransformed to cancer cells via a positive feedback loop involving NF-kappaB, Lin28, let-7, and IL-6. We identify differentially regulated microRNAs important for this switch and putative transcription factor binding sites in …
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Authors Iliopoulos D;Jaeger SA;Hirsch HA;Bulyk ML;Struhl K;;
Journal molecular cell
Year 2010
DOI DOI not found
URL
https://www.ncbi.nlm.nih.gov/pubmed/20797623
Keywords
National Center for Biotechnology Information NCBI NLM MEDLINE genetic Mice gene expression regulation animals humans pubmed abstract nih national institutes of health national library of medicine research support algorithms female N.I.H. Extramural Proto-Oncogene Proteins c-akt / metabolism Genes genetic* Receptors Promoter Regions micrornas / metabolism* kinetics computational biology cell movement nude breast neoplasms / pathology signal transduction inflammation / genetics transfection neoplasm invasiveness cell proliferation cell transformation colonic neoplasms / genetics colonic neoplasms / metabolism epigenesis neoplastic inflammation mediators / metabolism adenocarcinoma / therapy estrogen / genetics transcriptional activation tumor suppressor proteins / genetics rna interference binding sites nf-kappa b / metabolism stat3 transcription factor / metabolism* xenograft model antitumor assays tumor burden mammary glands human / pathology neoplastic / pathology neoplastic / genetics adenocarcinoma / metabolism proto-oncogene proteins c-myc / genetics human / metabolism* pmid:20797623 pmc2929389 doi:10.1016/j.molcel.2010.07.023 dimitrios iliopoulos savina a jaeger kevin struhl adenocarcinoma / genetics breast neoplasms / genetics breast neoplasms / metabolism* neoplastic / metabolism* colonic neoplasms / therapy deubiquitinating enzyme cyld src hct116 cells ht29 cells inflammation / metabolism* pten phosphohydrolase / metabolism* proto-oncogene proteins c-myc / metabolism tumor suppressor proteins / metabolism*

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