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The activating transcription factor 2: an influencer of cancer progression
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SYSNO ASEP 0522727 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title The activating transcription factor 2: an influencer of cancer progression Author(s) Huebner, K. (DE)
Procházka, Jan (UMG-J) ORCID
Monteiro, Ana C. (DE)
Mahadevan, V. (IN)
Schneider-Stock, R. (DE)Number of authors 5 Source Title Mutagenesis. - : Oxford University Press - ISSN 0267-8357
Roč. 34, č. 5-6 (2019), s. 375-389Number of pages 15 s. Publication form Online - E Language eng - English Country GB - United Kingdom Keywords amp response element ; n-terminal kinase ; c-jun gene ; dna-binding ; down-regulation ; protein-kinase ; poor-prognosis ; melanoma-cells ; intramolecular inhibition ; tumor progression Subject RIV EB - Genetics ; Molecular Biology OECD category Developmental biology R&D Projects LM2015040 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) EF16_013/0001789 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) ED1.1.00/02.0109 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) ED2.1.00/19.0395 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) Method of publishing Open access Institutional support UMG-J - RVO:68378050 UT WOS 000509474200003 DOI 10.1093/mutage/gez041 Annotation In contrast to the continuous increase in survival rates for many cancer entities, colorectal cancer (CRC) and pancreatic cancer are predicted to be ranked among the top 3 cancer-related deaths in the European Union by 2025. Especially, fighting metastasis still constitutes an obstacle to be overcome in CRC and pancreatic cancer. As described by Fearon and Vogelstein, the development of CRC is based on sequential mutations leading to the activation of proto-oncogenes and the inactivation of tumour suppressor genes. In pancreatic cancer, genetic alterations also attribute to tumour development and progression. Recent findings have identified new potentially important transcription factors in CRC, among those the activating transcription factor 2 (ATF2). ATF2 is a basic leucine zipper protein and is involved in physiological and developmental processes, as well as in tumorigenesis. The mutation burden of ATF2 in CRC and pancreatic cancer is rather negligible, however, previous studies in other tumours indicated that ATF2 expression level and subcellular localisation impact tumour progression and patient prognosis. In a tissue- and stimulus-dependent manner, ATF2 is activated by upstream kinases, dimerises and induces target gene expression. Dependent on its dimerisation partner, ATF2 homodimers or heterodimers bind to cAMP-response elements or activator protein 1 consensus motifs. Pioneering work has been performed in melanoma in which the dual role of ATF2 is best understood. Even though there is increasing interest in ATF2 recently, only little is known about its involvement in CRC and pancreatic cancer. In this review, we summarise the current understanding of the underestimated 'cancer gene chameleon' ATF2 in apoptosis, epithelial-to-mesenchymal transition and microRNA regulation and highlight its functions in CRC and pancreatic cancer. We further provide a novel ATF2 3D structure with key phosphorylation sites and an updated overview of all so-far available mouse models to study ATF2 in vivo. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2020 Electronic address https://academic.oup.com/mutage/article/34/5-6/375/5651345
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