Methylation Status Of The PCDH17Gene Promoter In Nasopharyngeal Carcinoma

Objective To investigate PCDH17gene promoter methylation statusand its impact on the transcriptional expression of PCDH17in NPC(Nasopharyngeal carcinoma, NPC) cell lines. and to investigate thefunction of PCDH17in nasopharyngeal carcinoma.Methods Semi-quantitative reverse transcription PCR (reversetranscription polymerase Chain PCR,RT-PCR) and Methylation specificPCR(Methylation-specific PCR, MSP) were used not only to detecttranscription level and promoter methylation status of PCDH17gene infive NPC cell lines, human laryngeal carcinoma cell line (Fadu), normalimmortalized epithelial cell lines (NP69),and NPC tissues, normal tissuesbut also after NPC cell lines were exposed to demethylating agent. Thetumor-suppressive function of PCDH17in NPC cancer was investigatedfurther in vitro assays.Results The expression of PCDH17mRNA was found in NP69butnot found in5NPC cell lines. Methylation specific PCR analysis revealedthat the PCDH17promoter was highly methylated in100％（5/5）of NPC cell lines,83.3%(35of42) of primary tumors, whereas only17.6％（3of17）of Non-malignant nasopharynx tissues exhibited hypermethylation inthe PCDH17promoter region.Demethylating agent could restore theexpression of PCDH17mRNA.The Cell function experiments suggest thatPCDH17could inhibit the cell colony formation and migration.Conclusion The transcriptional inactivation in NPC cell lines ismainly caused by the PCDH17DNA CPG-island methylation. PCDH17plays a role of tumor suppressor gene in NPC.