4.8 Editorial Material

Claudin-1 as a promoter of EMT in hepatocellular carcinoma

Journal

ONCOGENE
Volume 32, Issue 41, Pages 4871-4872

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2012.591

Keywords

Claudin-1; hepatocellular cancer; invasion; Ras; ERK; c-Abl

Funding

  1. Cancer Research UK Funding Source: Medline
  2. Department of Health [NIHR-RP-011-053] Funding Source: Medline
  3. Cancer Research UK [14549] Funding Source: researchfish
  4. National Institute for Health Research [NIHR-RP-011-053] Funding Source: researchfish

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Claudins are integral structural and functional components of apical cell adhesions (tight junctions). Loss of such adhesions has been associated with malignant transformation, a process most often accompanied by a concomitant loss of claudin expression. A growing body of evidence reveals the highly contextual upregulation of claudin expression in certain cancer types, and moreover their relevance in promoting cancer cell invasion and metastatic progression. In this issue of Oncogene, Suh et al. reported on claudin-1 expression in hepatocellular carcinoma (HCC), including its role as a promoter of the epithelial - to - mesenchymal transition via the c-Abl/Raf/Ras/ERK signaling pathway. Considering the limited therapeutic options in HCC, evaluation of its role as a target merits further investigation.

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