Reduced expression of multiple gap junction proteins is a feature of cervical dysplasia

Trond Aasen¹^,2^,3 , Sheila V Graham² , Mike Edward¹ and Malcolm B Hodgins¹

¹Squamous Cell Biology and Dermatology, Division of Cancer Sciences and Molecular Pathology, Robertson Building, University of Glasgow, 56 Dumbarton Road, Glasgow, G11 6NU, Scotland, UK

²Institute of Biomedical and Life Sciences, Division of Virology, University of Glasgow, Church Street, Glasgow, G11 6JR, Scotland, UK

³Centre for Cutaneous Research, Institute of Cell and Molecular Science, Queen Mary University of London, 4 Newark Street, Whitechapel, London E1 2AT, UK

author email corresponding author email

Molecular Cancer 2005, 4:31doi:10.1186/1476-4598-4-31


Published:	9 August 2005

Abstract

Cervical dysplasia is a premalignant lesion associated with human papillomavirus (HPV) infection which, over time, can turn cancerous. Previous studies have indicated that loss of gap junctions may be a feature of cervical cancer and premalignant dysplasia. Loss of the gap junction protein connexin43 has been demonstrated in dysplastic cervix, but other connexins have not been investigated. In contrast we previously showed that HPV-associated cutaneous warts – and other hyperproliferative skin conditions – display a dramatic upregulation of certain connexins, in particular connexin26. By performing immunofluorescence staining after antigen retrieval of paraffin-embedded cervical tissue samples, this study reports for the first time that connexin26 and connexin30, in addition to connexin43, are expressed in differentiating cells of normal human cervical epithelia. Moreover, in dysplastic ectocervix, all connexins studied display a dramatic loss of expression compared to adjacent normal epithelia. The role of connexins in keratinocyte differentiation and carcinogenesis is discussed.