Thus, it is conceivable that the external K(+) concentration in EL is a key environmental factor to regulate the survival of exogenous stem cells. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Purpose: Identifying tumor suppressor genes silenced by promoter CpG methylation uncovers mechanisms of tumorigenesis and identifies new epigenetic biomarkers for early cancer detection. DLEC1 is located at 3p22.3, www.selleckchem.com/products/Trichostatin-A.html a critical tumor suppressor gene locus for renal cell carcinoma. We explored its epigenetic alteration in renal cell carcinoma and possible clinicopathological association.
Materials and Methods: We examined
DLEC1 expression and methylation by semiquantitative reverse transcriptase and methylation specific polymerase chain reaction in 9 renal cell carcinoma cell lines and 81 primary tumors. We also analyzed the relationship between DLEC1 methylation and clinicopathological features in patients with renal
cell carcinoma. We assessed DLEC1 inhibition of renal cell carcinoma cell growth by colony formation assay.
Results: DLEC1 methylation and down-regulation were detected in all renal cell carcinoma cell lines. Treatment with 5-aza-2′-deoxycytidine (Sigma (R)) and/or trichostatin A (Cayman Chemical, Ann Arbor, Selleckchem Lonafarnib Michigan) reversed methylation and restored DLEC1 expression, indicating that methylation directly mediates its silencing. Aberrant methylation was further detected Amrubicin in 25 of 81 primary tumors (31%) but only 1 of 53 nonmalignant renal tissues (2%) showed methylation. DLEC1 methylation status was significantly associated with TNM classification
and grade in patients with renal cell carcinoma (chi-square test p = 0.01 and 0.04, respectively). DLEC1 ectopic expression in silenced renal cell carcinoma cells resulted in substantial tumor cell clonogenicity inhibition.
Conclusions: To our knowledge we report for the first time that DLEC1 is often down-regulated by CpG methylation and shows tumor inhibitory function in renal cell carcinoma cells, indicating its role as a tumor suppressor. DLEC1 tumor specific methylation may serve as a biomarker for early detection and prognosis prediction of this tumor.”
“The pathogenesis of Alzheimer’s disease (AD) senile plaque (SP) and neurofibrillary tangle (NFT) lesions putatively involves a compromised blood-brain barrier (BBB). P-glycoprotein (P-gp) is a recognized BBB-related efflux transporter protein. In this investigation we determined the density of SP and NFT lesions and capillary densities stained positively for P-glycoprotein (P-gp), and other transport proteins, in AD and control group (CG) brain samples. Our results indicate that there are significant negative correlations (p < .01) between the densities of NFT and SP(40) lesions and P-gp positive capillaries in AD but not CG brain samples. Significant positive correlations (p < .