Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that promoter hypermethylation plays a key role in DLC-1 inactivation in nasopharyngeal carcinoma (NPC). However, DLC-1 mutation in NPC has not been reported, and there remain some discrepancies in methods and results between different groups. Here, we examined the mRNA and protein expression of DLC-1 in chronic nasopharyngitis (CN) and NPC tissues by reverse transcription-polymerase chain reaction/qPCR and immunohistochemistry, respectively. DLC-1 mRNA was undetectable in all the seven widely used NPC cell lines and absent or significantly down-regulated in 70% of NPC tissues. DLC-1 protein level was reduced in 74.3% of NPCs when compared with CN tissues, and significantly lower in NPC samples at advanced clinical stages than that at early stages. Then, we purified the same batch of specimens by microdissection and analyzed the possible mechanisms of DLC-1 downregulation with mutation and allelic loss analysis, methylation-specific PCR and bisulfite genomic sequencing. Only one mutation was detected at codon 693 of exon 8 in 3.3% of NPCs and five single nucleotide polymorphisms (SNPs) were identified. Loss of DLC-1 was detected in 23.3% of NPC tissues. The 100% of NPC cell lines, 80% of primary NPC and 22.2% of CN tissues showed methylation in DLC-1 promoter, while DLC-1 expression was recovered in seven NPC cell lines after 5-aza-dC treatment. Patched methylation assay confirmed that promoter methylation could repress DLC-1 expression. This report demonstrates that DLC-1 is negatively associated with NPC carcinogenesis, and promoter hypermethylation along with loss of heterozygosity, but not mutation, contributes to inactivation of DLC-1 in NPC.
Mol Carcinog 2014 Nov
PMID:Promoter hypermethylation along with LOH, but not mutation, contributes to inactivation of DLC-1 in nasopharyngeal carcinoma. 2390 59

The aim of this study was to investigate the expression of LRRC4 in nasopharyngeal carcinomas, nasopharyngeal precancerous lesions, and nasopharyngitis as well as the clinical significance of LRRC4. Fifty patients with nasopharyngeal carcinoma were selected as study subjects; 28 patients with chronic nasopharyngitis and 22 patients with nasopharyngeal precancerous lesions served as controls. Immunohistochemical analysis was used to study protein expression of LRRC4; the relation between LRRC4 expression and the clinical stage and histopathological features of nasopharyngeal carcinoma was also analyzed. The LRRC4 expression manifested itself as yellow staining in the cytoplasm or nucleus. LRRC4 was strongly expressed in nasopharyngeal epithelial tissues of patients with chronic nasopharyngitis and in nasopharyngeal precancerous lesions; the rates of positive results were 82.1 and 81.8%, respectively. LRRC4 was weakly expressed in nasopharyngeal carcinoma tissues, at a rate of 10% positive results (P< 0.001); there was no significant difference in the expression of LRRC4 among different clinical stages and pathological grades. Therefore, disappearance of LRRC4 expression is a major feature of nasopharyngeal carcinoma.
Genet Mol Res 2015 Dec 09
PMID:Expression and clinical significance of LRRC4 in benign and malignant nasopharyngeal diseases. 2666 36

The gene glutamate receptor, ionotropic, N-methyl D-aspartate 2A (GRIN2A) is associated with development and neuron viability, and our previous studies showed it to be substantially methylated in nasopharyngeal carcinoma, indicating a link to this disease. The aim of this work was to investigate GRIN2A expression and its clinical significance in nasopharyngeal carcinoma, in contrast to nasopharyngitis and nasopharyngeal precancerous lesions. Fifty patients with nasopharyngeal carcinoma were selected as study subjects, while 28 chronic nasopharyngitis patients and 22 individuals with nasopharyngeal precancerous lesions were used as controls. Immunohistochemical analysis was used to study GRIN2A protein expression, and its relationship with nasopharyngeal carcinoma clinical stage and histopathological features were assessed. GRIN2A appeared as yellow staining in the cytoplasm or nucleus. It was strongly expressed in the nasopharyngeal epithelial tissues of patients with chronic nasopharyngitis and in nasopharyngeal precancerous lesions, the proportions of GRIN2A-positive cells being 82.1 and 72.7%, respectively. However, it was weakly expressed in nasopharyngeal carcinoma tissues, with 28.0% of cells testing positive (P < 0.001). No significant difference in the expression of GRIN2A was observed between different clinical stages and pathological grades. We conclude that weak GRIN2A expression is a major feature of nasopharyngeal carcinoma.
Genet Mol Res 2015 Dec 17
PMID:Expression of GRIN2A in benign and malignant nasopharyngeal diseases and its clinical significance. 2668 Dec 23