Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43146 (tumour suppressor)
 5,935 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The normal epithelial cell-specific 1 (NES1) gene (official name kallikrein gene 10; KLK10) is a new member of the expanding human kallikrein gene family and encodes for a secreted serine protease. Experimental evidence suggests that NES1 controls normal cell growth and may function as a tumour suppressor. NES1 is down-regulated during breast cancer progression. The NES1 gene is highly expressed in testicular as well as in other tissues. In this study, we investigated the expression level of the NES1 gene in cancerous and normal testicular tissues with reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. In all 14 primary testicular germ-cell tumours examined, the NES1 gene expression was markedly reduced compared to adjacent (paired) normal tissues. We further examined 6 randomly selected primary germ-cell tumours and 8 normal tissues (obtained from different individuals). We confirmed the differential expression of the NES1 gene in germ-cell tumours (GCT) and pre-malignant carcinoma in situ (CIS). Our findings suggest that NES1 may act as a tumour suppressor and may play a role in the pathogenesis and progression of this malignancy.
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PMID:Expression of the normal epithelial cell-specific 1 (NES1; KLK10) candidate tumour suppressor gene in normal and malignant testicular tissue. 1146 Oct 80

Tissue kallikrein (KLK1) and plasma kallikrein (KLKB1) may regulate the growth and proliferation of tumours of the lung and pleura, through the generation of kinin peptides that signal through the kinin B(1) (BDKRB1) and B(2) (BDKRB2) receptors. The development and progression of cancer results from genetic mutations, as well as epigenetic changes that include methylation of DNA at CpG islands. The aim of this study was to assess whether expression of the kallikrein-kinin genes in lung cancer and mesothelioma cells is regulated by DNA methylation. Quantitative reverse transcriptase-PCR and immunocytochemistry showed differences in the basal expression of the kallikrein-kinin genes and proteins in lung carcinoma and mesothelioma cells, compared with non-malignant lung epithelial and mesothelial cells, respectively. Following treatment with the demethylating agent, 5-azacytidine (5-AZA), KLKB1 mRNA expression was consistently increased in both lung carcinoma and mesothelioma cells, whereas KLK1, BDKRB1 and BDKRB2 mRNA expression was decreased or unchanged. Increased expression of KLKB1 after 5-AZA treatment suggests it may function as a tumour suppressor gene in cancers of the lung and pleura. Studies on DNA methylation of the kallikrein-kinin genes will enhance understanding of their role in carcinogenesis and provide insights into the importance of kallikreins as tumour biomarkers.
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PMID:Effects of the demethylating agent, 5-azacytidine, on expression of the kallikrein-kinin genes in carcinoma cells of the lung and pleura. 2190 90