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JUNB governs a feed-forward network of TGF beta signaling that aggravates breast cancer invasion
Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Univ Tokyo, Grad Sch Med, Dept Mol Pathol, Tokyo 1130033, Japan..
Leiden Univ, Med Ctr, Canc Genom Ctr Netherlands, Dept Mol Cell Biol, POB 9600, NL-2300 RC Leiden, Netherlands..
Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
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2018 (engelsk)Inngår i: Nucleic Acids Research, ISSN 0305-1048, E-ISSN 1362-4962, Vol. 46, nr 3, s. 1180-1195Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

It is well established that transforming growth factor-beta (TGF beta) switches its function from being a tumor suppressor to a tumor promoter during the course of tumorigenesis, which involves both cell-intrinsic and environment-mediated mechanisms. We are interested in breast cancer cells, in which SMAD mutations are rare and interactions between SMAD and other transcription factors define pro-oncogenic events. Here, we have performed chromatin immunoprecipitation (ChIP)-sequencing analyses which indicate that the genome-wide landscape of SMAD2/3 binding is altered after prolonged TGF beta stimulation. De novo motif analyses of the SMAD2/3 binding regions predict enrichment of binding motifs for activator protein (AP) 1 in addition to SMAD motifs. TGF beta-induced expression of the AP1 component JUNB was required for expression of many late invasion-mediating genes, creating a feed-forward regulatory network. Moreover, we found that several components in the WNT pathway were enriched among the late TGF beta-target genes, including the invasion-inducing WNT7 proteins. Consistently, overexpression of WNT7A or WNT7B enhanced and potentiated TGF beta-induced breast cancer cell invasion, while inhibition of the WNT pathway reduced this process. Our study thereby helps to explain how accumulation of pro-oncogenic stimuli switches and stabilizes TGF beta-induced cellular phenotypes of epithelial cells.

sted, utgiver, år, opplag, sider
OXFORD UNIV PRESS , 2018. Vol. 46, nr 3, s. 1180-1195
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URN: urn:nbn:se:uu:diva-349356DOI: 10.1093/nar/gkx1190ISI: 000425294400020PubMedID: 29186616OAI: oai:DiVA.org:uu-349356DiVA, id: diva2:1202904
Forskningsfinansiär
Swedish Cancer Society, 09 0773, 10 0452, 2016/445Swedish Research Council, 2015-02757Tilgjengelig fra: 2018-05-02 Laget: 2018-05-02 Sist oppdatert: 2018-05-02bibliografisk kontrollert

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