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Distinct P‐cadherin expression in cultured normal human keratinocytes and squamous cell carcinoma cell lines
Author(s) -
Wakita Hisashi,
Shirahama Shigeho,
Furukawa Fukumi
Publication year - 1998
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/(sici)1097-0029(19981101)43:3<218::aid-jemt3>3.0.co;2-s
Subject(s) - cadherin , extracellular , cell , cell culture , microbiology and biotechnology , keratinocyte , biology , cancer cell , chemistry , cancer research , cancer , biochemistry , genetics
Spatially regulated expression of E (epithelial)‐ and P (placental)‐cadherins is crucial for maintaining normal epidermal architecture. In cutaneous squamous cell carcinomas (SCCs), aberrant P‐cadherin expression is often observed in “squamoid” cancer cells, whereas E‐cadherin expression in cancer cells is generally reduced. Therefore, it is plausible that SCC cells have acquired the ability to express P‐cadherin and that P‐cadherin plays a role in tumor progression. To address the issue, the in vitro effect of extracellular calcium on differentiation is a good model for investigating P‐cadherin in normal and neoplastic skin. With elevations in extracellular calcium, human SCC cell line (DJM‐1) cells initiate de novo synthesis of P‐cadherin and express P‐cadherin on the cell surface, whereas in normal human keratinocytes, P‐cadherin expression on the cell surface is enhanced via the translocation from the cytosol to the cell membrane and/ or the stabilization of P‐cadherin at the cell surface. DJM‐1 cells maintain P‐cadherin expression on the cell surface at high levels for over 4 days after calcium elevation, whereas normal human keratinocytes cannot sustain cell surface P‐cadherin when the cells are cultured in high calcium for more than 2 days. P‐cadherin synthesis in DJM‐1 cells is regulated at translational levels by extracellular calcium concentrations. SCC cells have the ability to produce P‐cadherin by a mechanism not observed in normal keratinocytes, which might relate to the aberrant expression of P‐cadherin in SCC of the skin. Microsc. Res. Tech. 43:218–223, 1998. © 1998 Wiley‐Liss, Inc.