Collagen XVII is expressed in malignant but not in benign melanocytic tumors and it can mediate antibody induced melanoma apoptosis

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• 作者：T. Krenacs (1) krenacst@gmail.com
  G. Kiszner (1)
  E. Stelkovics (2)
  P. Balla (1)
  I. Teleki (1)
  I. Nemeth (3)
  E. Varga (3)
  I. Korom (3)
  T. Barbai (4)
  V. Plotar (5)
  J. Timar (4)
  E. Raso (4)
• 关键词：Collagen XVII endodomain – ; Malignant melanoma – ; Borderline dysplastic lesions – ; Melanoma invasion – ; Antibody ; induced apoptosis
• 刊名：Histochemistry and Cell Biology
• 出版年：2012
• 出版时间：October 2012
• 年：2012
• 卷：138
• 期：4
• 页码：653-667
• 全文大小：1.7 MB
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• 作者单位：1. 1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Ulloi ut 26, Budapest, 1085 Hungary2. Laboratory of Tumor Pathology and Molecular Diagnostics, Bay Zoltan Foundation for Applied Research, Szeged, Hungary3. Department of Dermatology and Allergology, University of Szeged, Szeged, Hungary4. 2nd Department of Pathology, Semmelweis University, Budapest, Hungary5. Oncopathology Department, National Institute of Oncology, Budapest, Hungary
• ISSN：1432-119X

文摘

The 180 kDa transmembrane collagen XVII is known to anchor undifferentiated keratinocytes to the basement membrane in hemidesmosomes while constitutively shedding a 120 kDa ectodomain. Inherited mutations or auto-antibodies targeting collagen XVII cause blistering skin disease. Collagen XVII is down-regulated in mature keratinocytes but re-expressed in skin cancer. By recently detecting collagen XVII in melanocyte hyperplasia, here we tested its expression in benign and malignant melanocytic tumors using endodomain and ectodomain selective antibodies. We found the full-length collagen XVII protein in proliferating tissue melanocytes, basal keratinocytes and squamous cell carcinoma whereas resting melanocytes were negative. Furthermore, the cell-residual 60 kDa endodomain was exclusively detected in 62/79 primary and 15/18 metastatic melanomas, 8/9 melanoma cell lines, HT199 metastatic melanoma xenografts and atypical nests in 8/63 dysplastic nevi. The rest of 19 nevi including common, blue and Spitz subtypes were also negative. In line with the defective ectodomain, sequencing of COL17A1 gene revealed aberrations in the ectodomain coding region including point mutations. Collagen XVII immunoreaction-stained spindle cell melanomas, showed partly overlapping profiles with those of S100B, Melan A and HMB45. It was concentrated at vertical melanoma fronts and statistically associated with invasive phenotype. Antibody targeting the extracellular aa507–529 terminus of collagen XVII endodomain promoted apoptosis and cell adhesion, while inhibiting proliferation in HT199 cells. These results suggest that the accumulation of collagen XVII endodomain in melanocytic tumors is associated with malignant transformation to be a potential marker of malignancy and a target for antibody-induced melanoma apoptosis.