PRK, a cell cycle gene localized to 8p21, is downregulated in head and neck cancer

• Published in: Genes chromosomes & cancer 2000-03, Vol.27 (3), p.332-336
• Main Authors: Dai, Wei, Li, Yaqin, Ouyang, Bin, Pan, Huiqi, Reissmann, Peter, Li, Jian, Wiest, Jonathan, Stambrook, Peter, Gluckman, Jack L., Noffsinger, Amy, Bejarano, Pablo
• Format: Article
• Language: English
• Subjects: Carcinoma, Squamous Cell - genetics; Chromosome Mapping; Chromosomes, Human, Pair 8 - genetics; Down-Regulation - genetics; Genes, cdc - physiology; Head and Neck Neoplasms - genetics; Humans; Protein Kinase C; Protein-Serine-Threonine Kinases - biosynthesis; Protein-Serine-Threonine Kinases - genetics; RNA, Messenger - biosynthesis
• ISSN: 1045-2257; 1098-2264
• DOI: 10.1002/(SICI)1098-2264(200003)27:3<332::AID-GCC15>3.0.CO;2-K

The human PRK gene encodes a protein serine/threonine kinase of the polo family and plays an essential role in regulating meiosis and mitosis. We have previously shown that PRK expression is downregulated in a significant fraction of lung carcinomas. Our current studies reveal that PRK mRNA expression is downregulated in a majority (26 out of 35 patients) of primary head and neck squamous‐cell carcinomas (HNSCC) compared with adjacent uninvolved tissues from the same patients, regardless of stage. In addition, PRK transcripts were undetectable in one of the two HNSCC cell lines analyzed. Ectopic expression of PRK, but not a PRK deletion construct, in transformed A549 fibroblast cells suppresses their proliferation. Furthermore, fluorescence in situ hybridization analyses show that the PRK gene localizes to chromosome band 8p21, a region that exhibits a high frequency of loss of heterozygosity in a variety of human cancers, including head and neck cancers, and that is proposed to contain two putative tumor suppressor genes. Considering that PRK plays an important role in the regulation of the G2/M transition and cell cycle progression, our current studies suggest that deregulated expression of PRK may contribute to tumor development. Genes Chromosomes Cancer 27:332–336, 2000. © 2000 Wiley‐Liss, Inc.