Promoter hypermethylation of CCNA1 , RARRES1 , and HRASLS3 in nasopharyngeal carcinoma

• Published in: Oral oncology Vol. 44; no. 4; pp. 400 - 406
• Main Authors: Yanatatsaneejit, Pattamawadee, Chalermchai, Thep, Kerekhanjanarong, Veerachai, Shotelersuk, Kanjana, Supiyaphun, Pakpoom, Mutirangura, Apiwat, Sriuranpong, Virote
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01-04-2008; Elsevier
• Subjects: Biological and medical sciences; Cyclin A - genetics; Cyclin A1; DNA Methylation; DNA, Neoplasm - genetics; Gene Expression Profiling - methods; Genes, Tumor Suppressor; Hematology, Oncology and Palliative Medicine; HRASLS3; Humans; Intracellular Signaling Peptides and Proteins - genetics; Loss of Heterozygosity; Medical sciences; Membrane Proteins - genetics; Nasopharyngeal carcinoma; Nasopharyngeal Neoplasms - genetics; Neoplasm Proteins - genetics; Otolaryngology; Otorhinolaryngology. Stomatology; Phospholipases A2, Calcium-Independent; Polymerase Chain Reaction - methods; Promoter hypermethylation; Promoter Regions, Genetic - genetics; RARRES1; Tumor Cells, Cultured; Tumor suppressor gene; Tumor Suppressor Proteins - genetics; Tumors; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology; NPC; CCNA1; retinoic acid receptor responsive element; nasopharyngeal carcinoma; Promoter hypermethylation; RARRES1; HRASLS3; h-RAS like suppressor; cyclin A1; Tumor suppressor gene; Nasopharyngeal carcinoma; Cyclin A1; Transcription promoter; Stomatology; ENT; Malignant tumor; Nasopharynx carcinoma; Cancerology; ENT disease; Pharynx disease; RARRES1;HRASLS3; Cancer
• ISSN: 1368-8375; 1879-0593
• DOI: 10.1016/j.oraloncology.2007.05.008

Summary In search for putative tumor suppressor genes critical of nasopharyngeal carcinoma (NPC), we analyzed the available information from the expression profiling in conjunction with the comprehensive alleotyping published data relevant to this malignancy. Integration of this information suggested eight potential candidate tumor suppressor genes, CCNA1 , HRASLS3 , RARRES1 , CLMN , EML1 , TSC22 , LOH11CR2A and MCC . However, to confirm the above observations, we chose to investigate if promoter hypermethylation of these candidate genes would be one of the mechanisms responsible for the de-regulation of gene expression in NPC in addition to the loss of genetic materials. In this study, we detected consistent hypermethylation of the 5′ element of CCNA1 , RARRES1 , and HRASLS in NPC tissues with prevalence of 48%, 51%, and 17%, respectively. Moreover, we found a similar profile of promoter hypermethylation in primary cultured NPC cells but none in normal nasopharyngeal epithelium or leukocytes, which further substantiate our hypothesis. Our data indicate that CCNA1 , RARRES1 , and HRASLS3 may be the putative tumor suppressor genes in NPC.