A1 Refereed original research article in a scientific journal
Expression of claudin-11 by tumor cells in cutaneous squamous cell carcinoma is dependent on the activity of p38δ
Authors: Nissinen L, Siljamaki E, Riihila P, Piipponen M, Farshchian M, Kivisaari A, Kallajoki M, Raiko L, Peltonen J, Peltonen S, Kahari VM
Publisher: WILEY
Publication year: 2017
Journal: Experimental Dermatology
Journal name in source: EXPERIMENTAL DERMATOLOGY
Journal acronym: EXP DERMATOL
Volume: 26
Issue: 9
First page : 771
Last page: 777
Number of pages: 7
ISSN: 0906-6705
DOI: https://doi.org/10.1111/exd.13278
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/26622339
The incidence of cutaneous squamous cell carcinoma (cSCC) is rapidly increasing, and the prognosis of patients with metastatic disease is poor. There is an emerging need to identify molecular markers for predicting aggressive behaviour of cSCC. Here, we have examined the role of tight junction (TJ) components in the progression of cSCC. The expression pattern of mRNAs for TJ components was determined with RNA sequencing and oligonucleotide array-based expression analysis from cSCC cell lines (n=8) and normal human epidermal keratinocytes (NHEK, n=5). The expression of CLDN11 was specifically elevated in primary cSCC cell lines (n=5), but low or absent in metastatic cSCC cell lines (n=3) and NHEKs. Claudin-11 was detected in cell-cell contacts of primary cSCC cells in culture by indirect immunofluorescence analysis. Analysis of a large panel of tissue samples from sporadic UV-induced cSCC (n=65), cSCC in situ (n=56), actinic keratoses (n=31), seborrhoeic keratoses (n=7) and normal skin (n=16) by immunohistochemistry showed specific staining for claudin-11 in intercellular junctions of keratinizing tumor cells in well and moderately differentiated cSCCs, whereas no staining for claudin-11 was detected in poorly differentiated tumors. The expression of claudin-11 in cSCC cells was dependent on the activity of p38 delta MAPK and knock-down of claudin-11 enhanced cSCC cell invasion. These findings provide evidence for the role of claudin-11 in regulation of cSCC invasion and suggest loss of claudin-11 expression in tumor cells as a biomarker for advanced stage of cSCC.
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