Promoter methylation and inactivation of tumour-suppressor genes in oral squamous-cell carcinoma

Methylation status of breast cancer resistance protein detected by methylation‐specific polymerase chain reaction analysis is correlated inversely with its expression in drug‐resistant lung cancer cells

“…[40][41][42][43][44] In those studies, the high sensitivity and specificity of MSP successfully allowed accurate detection of the inactivation of tumor suppressor genes. We also have developed the MSP method to detect promoter methylation of BCRP.…”

PRTFDC1, a possible tumor-suppressor gene, is frequently silenced in oral squamous-cell carcinomas by aberrant promoter hypermethylation

“…Consequently, the methylation status of PRTFDC1 is unlikely to correlate with tumor behavior, although information on patient outcome was not available. However, among various TSGs, such as CDKN2B and 2A, CDH1, DAPK1, MGMT and DCC, whose methylation is known to be important in the development of OSCC (Ha and Califano, 2006;Shaw, 2006), only a few reports have shown a correlation between the methylation status of those genes and clinicopathological characteristics or prognosis (Shaw, 2006). Since there may be the potential for therapeutic and/or diagnostic advantages if specific aberrations could be shown to correlate with tumor behavior, further study using a larger set of cases, especially early Silencing of PRTFDC1 in oral cancer E Suzuki et al stage tumors, will be necessary for those methylationtarget genes including PRTFDC1 in OSCC.…”

“…A more comprehensive understanding of the molecular pathogenesis of OSCC is urgently needed to identify new targets and strategies for effective therapy, and the opportunity to recognize early OSCC and/or premalignant lesions may provide insight into the phase of new strategies for chemoprevention of this disease (Nagpal and Das, 2003;Brinkman and Wong, 2006). Although OSCC is believed to arise through the accumulation of numerous genetic and epigenetic alterations, which may impair the function of oncogenes or tumor suppressor genes (TSGs) that play a crucial role in the development of this disease (Scully et al, 2000;Ha and Califano, 2006), little is still known about the genes associated with oral carcinogenesis.…”

“…Indeed, epigenetic inactivation of TSGs, including DNA hypermethylation in their CpGrich promoter or exonic regions, has been believed to occur frequently and play important roles during the pathogenesis of human cancers, including oral cancer (Jones and Baylin, 2002;Ha and Califano, 2006). Hence, the mapping of homozygous deletions in OSCCs using high-throughput methods with high-resolution and sensitivity and further analyses of frequently inactivated 'driver genes' located within mapped regions may provide valuable clues for exploring OSCC-associated TSGs, even those whose inactivation occurs mainly by epigenetic mechanisms.…”

Effects of green tea polyphenol on methylation status of RECK gene and cancer cell invasion in oral squamous cell carcinoma cells

“…Recently, the decrease in RECK expression is reported to correlate with hypermethylation of the promoter region (Furumoto et al, 2000;Song et al, 2006;Chang et al, 2007;Cho et al, 2007). In human cancers, aberrant methylation of tumour suppressor genes is of comparable significance to classic genetic mutations (Lund and van Lohuizen, 2004;Ha and Califano, 2006;Stresemann et al, 2006;Shaw, 2006). The study of the patterns of gene silencing because of hypermethylation would therefore help to understand and predict cancer cell behaviour and responsiveness to various treatments of cancers (Hellebrekers et al, 2007;Shaw et al, 2007).…”