> Details

Eberl, Markus; Klingler, Stefan; Mangelberger, Doris; Loipetzberger, Andrea; Damhofer, Helene; Zoidl, Kerstin; Schnidar, Harald; Hache, Hendrik; Bauer, Hans‐Christian; Solca, Flavio; Hauser‐Kronberger, Cornelia; Ermilov, Alexandre N.; Verhaegen, Monique E.; Bichakjian, Christopher K.; Dlugosz, Andrzej A.; Nietfeld, Wilfried; Sibilia, Maria; Lehrach, Hans; Wierling, Christoph; Aberger, Fritz

Hedgehog‐EGFR cooperation response genes determine the oncogenic phenotype of basal cell carcinoma and tumour‐initiating pancreatic cancer cells

Reference
management

Bookmarks

Remove from
bookmarks

Share this on Whatsapp

Close

Bookmarks



You can manage bookmarks using lists, please log in to your user account for this.
  • Media type: E-Article
  • Title: Hedgehog‐EGFR cooperation response genes determine the oncogenic phenotype of basal cell carcinoma and tumour‐initiating pancreatic cancer cells
  • Contributor: Eberl, Markus; Klingler, Stefan; Mangelberger, Doris; Loipetzberger, Andrea; Damhofer, Helene; Zoidl, Kerstin; Schnidar, Harald; Hache, Hendrik; Bauer, Hans‐Christian; Solca, Flavio; Hauser‐Kronberger, Cornelia; Ermilov, Alexandre N.; Verhaegen, Monique E.; Bichakjian, Christopher K.; Dlugosz, Andrzej A.; Nietfeld, Wilfried; Sibilia, Maria; Lehrach, Hans; Wierling, Christoph; Aberger, Fritz
  • Published: Springer Science and Business Media LLC, 2012
  • Published in: EMBO Molecular Medicine, 4 (2012) 3, Seite 218-233
  • Language: English
  • DOI: 10.1002/emmm.201100201
  • ISSN: 1757-4676; 1757-4684
  • Origination:
  • Footnote:
  • Description: AbstractInhibition of Hedgehog (HH)/GLI signalling in cancer is a promising therapeutic approach. Interactions between HH/GLI and other oncogenic pathways affect the strength and tumourigenicity of HH/GLI. Cooperation of HH/GLI with epidermal growth factor receptor (EGFR) signalling promotes transformation and cancer cell proliferation in vitro. However, the in vivo relevance of HH‐EGFR signal integration and the critical downstream mediators are largely undefined. In this report we show that genetic and pharmacologic inhibition of EGFR signalling reduces tumour growth in mouse models of HH/GLI driven basal cell carcinoma (BCC). We describe HH‐EGFR cooperation response genes including SOX2, SOX9, JUN, CXCR4 and FGF19 that are synergistically activated by HH‐EGFR signal integration and required for in vivo growth of BCC cells and tumour‐initiating pancreatic cancer cells. The data validate EGFR signalling as drug target in HH/GLI driven cancers and shed light on the molecular processes controlled by HH‐EGFR signal cooperation, providing new therapeutic strategies based on combined targeting of HH‐EGFR signalling and selected downstream target genes.
  • Access State: Open Access