Regulation of G6PD acetylation by SIRT2 and KAT9 modulates NADPH homeostasis and cell survival during oxidative stress.

Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway (PPP) and plays an essential role in the oxidative stress response by producing NADPH, the main intracellular reductant. G6PD deficiency is the most common human enzyme defect, affecting more than 400 million people worldwide. Here, we show that G6PD is negatively regulated by acetylation on lysine 403 (K403), an evolutionarily conserved residue.

Unfavorable clinical implications of circulating CD44+ lymphocytes in patients with nasopharyngeal carcinoma undergoing radiochemotherapy.

Background: To evaluate the use of cellular immunity parameters as predictors of therapy response.

Methods: Circulating lymphocytes were measued by flow cytometry in 94 nasopharyngeal carcinoma (NPC) patients following radiochemotherapy.

Results: Significantly decreased percentage of CD3(+), CD4(+), and CD8(+) lymphocytes, significantly increased proportion of CD44(+), CD25(+), NK lymphocytes, and an increased CD4(+)/CD8(+) ratio were indicated in NPC patients as compared with healthy controls.

Hypermethylation-modulated downregulation of RASSF1A expression is associated with the progression of esophageal cancer.

Background And Aims: Chromosome 3p21 is an important locus harboring critical tumor suppressor genes (TSGs) implicated in the pathogenesis of multiple tumors including esophageal carcinoma (EC). Aberrant promoter methylation is a fundamental mechanism of inactivation of TSGs in cancer. RASSF1A, a candidate tumor suppressor gene, recently cloned from the lung tumor locus at 3p21.

Aberrant methylation of different DNA repair genes demonstrates distinct prognostic value for esophageal cancer.

Background: DNA mismatch repair (MMR) deficiency results in a strong mutator phenotype and high-frequency microsatellite instability (MSI-H), which are the hallmarks of many tumors.

Aim: The objective of this study is to investigate the promoter CpG island methylation status of mismatch repair genes human mutL homolog 1 (hMLH1), human mutS homolog 2 (hMSH2), and O(6)-methylguanine-DNA methyltransferase (MGMT) in esophageal squamous cell carcinoma (ESCC) and its roles in alkylating agents chemotherapy.

Methods: Real-time methylation-specific polymerase chain reaction (PCR) (real-time MSP) was employed to detect promoter CpG island methylation of the hMLH1, hMSH2, as well as MGMT genes in 235 surgical tumor tissue samples from ESCC patients and their corresponding normal tissue samples.

Hypermethylation-modulated down-regulation of CDH1 expression contributes to the progression of esophageal cancer.

CDH1, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation status of the CDH1 gene 5'-CpG islands and its regulatory mechanism in the progression of esophageal squamous cell carcinoma. Real-time methylation-specific polymerase chain reaction (qMSP) and treatment with the demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR) were conducted to analyze the methylation status at the CDH1 promoter region in the human esophageal carcinoma cell lines, EC1 and EC9706.