SOX9 regulates ERBB signalling in pancreatic cancer development

Grimont, Adrien; Pinho, Andreia V.; Cowley, Mark J.; Augereau, Cécile; Mawson, Amanda; Giry-Laterrière, Marc; Steen, Géraldine Van Den; Waddell, Nicola; Pajic, Marina; Sempoux, Christine; Wu, Jianmin; Grimmond, Sean M.; Biankin, Andrew V.; Lemaigre, Frédéric P.; Rooman, Ilse; Jacquemin, Patrick

doi:10.1136/gutjnl-2014-307075

Cited by 73 publications

(77 citation statements)

References 42 publications

(68 reference statements)

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“…Under inflammatory conditions, or in the presence of oncogenic KRAS, SOX9 is increasingly expressed in acinar cells and stimulates gene expression that leads to ADM 48 , development of pre-malignant lesions and initiation of PDAC in mice 14 . In line with these findings, SOX9 expression in patient tumour samples is elevated at all stages of preneoplastic lesions and PDAC 49 , correlating with increased expression of EGFR pathway-related genes 50 . Similarly, in mice, the absence of SOX9 reduces EGFR signalling and pancreatic tumorigenesis 50 .…”

Section: Acinar Cell Dedifferentiation Factorssupporting

confidence: 66%

“…In line with these findings, SOX9 expression in patient tumour samples is elevated at all stages of preneoplastic lesions and PDAC 49 , correlating with increased expression of EGFR pathway-related genes 50 . Similarly, in mice, the absence of SOX9 reduces EGFR signalling and pancreatic tumorigenesis 50 . However, EGFR signalling can also regulate expression of SOX9 through activation of NFATC1 and NFATC4 (REFS 51,52).…”

Section: Acinar Cell Dedifferentiation Factorssupporting

confidence: 66%

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Acinar cell plasticity and development of pancreatic ductal adenocarcinoma

Störz

2017

Nat Rev Gastroenterol Hepatol

265

273

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Acinar cells in the adult pancreas show high plasticity and can undergo transdifferentiation to a progenitor-like cell type with ductal characteristics. This process, termed acinar-to-ductal metaplasia (ADM), is an important feature facilitating pancreas regeneration after injury. Data from animal models show that cells that undergo ADM in response to oncogenic signalling are precursors for pancreatic intraepithelial neoplasia lesions, which can further progress to pancreatic ductal adenocarcinoma (PDAC). As human pancreatic adenocarcinoma is often diagnosed at a stage of metastatic disease, understanding the processes that lead to its initiation is important for the discovery of markers for early detection, as well as options that enable an early intervention. Here, the critical determinants of acinar cell plasticity are discussed, in addition to the intracellular and extracellular signalling events that drive acinar cell metaplasia and their contribution to development of PDAC.

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Section: Acinar Cell Dedifferentiation Factorssupporting

confidence: 66%

Section: Acinar Cell Dedifferentiation Factorssupporting

confidence: 66%

Acinar cell plasticity and development of pancreatic ductal adenocarcinoma

Störz

2017

Nat Rev Gastroenterol Hepatol

265

273

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“…According to recent literatures, ErbB signaling pathway and TGF-beta signaling pathway participate in the transmembrane signal transduction of pancreatic cancer [13, 14]. Such transmembrane signal transduction pathways have been further validated to transfer the signals to intracellular pathways (such as p53 signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, and VEGF signaling pathway) [13, 15–17]. Intracellular signaling pathways have been identified to contribute to the abnormal proliferation of pancreatic cells and further initiate the tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Important Gene Ontology Terms and Biological Pathways Related to Pancreatic Cancer

Yin

Wang

Zhang

et al. 2016

BioMed Research International

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Pancreatic cancer is a serious disease that results in more than thirty thousand deaths around the world per year. To design effective treatments, many investigators have devoted themselves to the study of biological processes and mechanisms underlying this disease. However, it is far from complete. In this study, we tried to extract important gene ontology (GO) terms and KEGG pathways for pancreatic cancer by adopting some existing computational methods. Genes that have been validated to be related to pancreatic cancer and have not been validated were represented by features derived from GO terms and KEGG pathways using the enrichment theory. A popular feature selection method, minimum redundancy maximum relevance, was employed to analyze these features and extract important GO terms and KEGG pathways. An extensive analysis of the obtained GO terms and KEGG pathways was provided to confirm the correlations between them and pancreatic cancer.

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“…In a study of pancreatic cancer, Sun et al found that the nuclear factor-κB signaling pathway can epigenetically regulate the expression of SOX9 and promote the invasiveness of CSCs (7). Grimont et al also demonstrated that SOX9 upregulated the ERBB signaling pathway to promote the tumorigenesis of pancreatic cancer (8). In addition, SOX9 is necessary for tumor cell initiation and division, self-renewal, and tumorigenicity in CSCs of hepatocellular carcinoma (9).…”

mentioning

confidence: 99%

“…Therefore, targeting of CSCs may be useful in cancer therapeutics. The crucial role played by SOX9 in CSCs has been verified in digestive system cancers, including pancreatic cancer and hepatocellular carcinoma (7)(8)(9). In a study of pancreatic cancer, Sun et al found that the nuclear factor-κB signaling pathway can epigenetically regulate the expression of SOX9 and promote the invasiveness of CSCs (7).…”

mentioning

confidence: 99%