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  • Result 1-4 of 4
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  • Grabner, B, et al. (author)
  • Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis
  • 2015
  • In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 6, s. 6285-
  • Journal article (peer-reviewed)abstract
    • STAT3 is considered to play an oncogenic role in several malignancies including lung cancer; consequently, targeting STAT3 is currently proposed as therapeutic intervention. Here we demonstrate that STAT3 plays an unexpected tumour-suppressive role in KRAS mutant lung adenocarcinoma (AC). Indeed, lung tissue-specific inactivation of Stat3 in mice results in increased KrasG12D-driven AC initiation and malignant progression leading to markedly reduced survival. Knockdown of STAT3 in xenografted human AC cells increases tumour growth. Clinically, low STAT3 expression levels correlate with poor survival and advanced malignancy in human lung AC patients with smoking history, which are prone to KRAS mutations. Consistently, KRAS mutant lung tumours exhibit reduced STAT3 levels. Mechanistically, we demonstrate that STAT3 controls NF-κB-induced IL-8 expression by sequestering NF-κB within the cytoplasm, thereby inhibiting IL-8-mediated myeloid tumour infiltration and tumour vascularization and hence tumour progression. These results elucidate a novel STAT3–NF-κB–IL-8 axis in KRAS mutant AC with therapeutic and prognostic relevance.
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  • Kuphal, S., et al. (author)
  • GLI1-dependent transcriptional repression of CYLD in basal cell carcinoma
  • 2011
  • In: Oncogene. - : Springer Science and Business Media LLC. - 1476-5594 .- 0950-9232. ; 30:44, s. 4523-4530
  • Journal article (peer-reviewed)abstract
    • CYLD is a deubiquitination enzyme that regulates different cellular processes, such as cell proliferation and cell survival. Mutation and loss of heterozygosity of the CYLD gene causes development of cylindromatosis, a benign tumour originating from the skin. Our study shows that CYLD expression is dramatically downregulated in basal cell carcinoma (BCC), the most common cancer in humans. Reduced CYLD expression in basal cell carcinoma was mediated by GLI1-dependent activation of the transcriptional repressor Snail. Inhibition of GLI1 restored the CYLD expression-mediated Snail signaling pathway, and caused a significant delay in the G1 to S phase transition, as well as proliferation. Our data suggest that GLI1-mediated suppression of CYLD has a significant role in basal cell carcinoma progression. Oncogene (2011) 30, 4523-4530; doi: 10.1038/onc.2011.163; published online 16 May 2011
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