Rey O, Baluda M A, Park N H
UCLA School of Dentistry and Dental Research Institute, Los Angeles, California 90095-1668, USA.
Oncogene. 1999 Jan 21;18(3):827-31. doi: 10.1038/sj.onc.1202328.
We have previously demonstrated that normal human oral keratinocytes immortalized by transfection with human papillomavirus type-16 Dna became tumorigenic after exposure to a chemical carcinogen. In an effort to detect differentially regulated genes associated with this transition from the immortal to the malignant phenotype, we employed representational differences analysis (a PCR-coupled subtractive hybridization technique). After analysing 50 colonies, 12 putative messages were identified. Northern analysis comparison using the identified cDNAs as probes was made between normal human oral keratinocyte, papillomavirus-immortalized human oral keratinocytes (HOK-16B), a neoplastic cell line derived from HOK-16B (HOK-16B-BaP-T) and the human oral cancer cell lines Hep-2, SCC-9 and Tu-177. We found that mRNAs encoding for cyclophilin A, c-myc binding protein 1, the heat shock protein 90alpha and one unknown transcript were up-regulated in the oral cancer cell lines analysed as well as in HOK-16B cells. We also detected a downregulation of the mRNAs encoding the skin-derived antileukoproteinase SKALP/elafin, the translationally regulated p23 protein and one unknown transcript. Whether these messages are associated to the neoplastic conversion of human keratinocytes remains to be determined.