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Human tenascin‐C: Identification of a novel type III repeat in oral cancer and of novel splice variants in normal, malignant and reactive oral mucosae
Author(s) -
Mighell Alan J.,
Thompson John,
Hume William J.,
Markham Alexander F.,
Robinson Philip A.
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970717)72:2<236::aid-ijc6>3.0.co;2-s
Subject(s) - alternative splicing , splice , tenascin , biology , tenascin c , cancer , rna splicing , kras , gene isoform , fibronectin , cancer research , microbiology and biotechnology , genetics , gene , extracellular matrix , colorectal cancer , rna
Tenascin‐C is a mosaic, linear glycoprotein that is up‐regulated during many normal and pathological processes involving either cell migration or tissue morphogenesis, such as invasion of malignant cells and wound healing. Human tenascin‐C contains 8 consecutive type III fibronectin (TNCfn) domains that are involved in alternative splicing and potentially generate a large number of isoforms that code for tenascin‐C proteins with subtly different functions. Human tenascin‐C splice variants were investigated by RT‐PCR in a range of normal and pathological oral mucosal tissues. A novel, 9th human TNCfn domain involved in alternative splicing was identified. It shares 70% nucleic acid and 55% protein sequence homology with chicken TNCfn‐ad2. As in avians, this novel repeat was located between TNCfn‐B and TNCfn‐ad1 and accordingly was designated human TNCfn‐ad2. Human TNCfn‐ad2 was detected in only 2 of 10 oral cancers. However, TNCfn‐ad2 was absent from 40 normal, reactive, pre‐malignant and other oral mucosal specimens investigated. Previous studies have described 8 splice variant transcripts for human tenascin‐C. By systematic investigation we identified further novel splice variants for human tenascin‐C. Furthermore, our results indicate that many potential splice variants probably do not exist in the tissues investigated. Thus, we have demonstrated that human tenascin‐C transcripts generate a complex but selected repertoire of different alternative splice products. Int. J. Cancer 72:236–240, 1997. © 1997 Wiley‐Liss, Inc.