Zolendronic acid shows its anticancer activity via apoptosis and autophagy. These findings can potentially contribute to the beneficial use of zolendronic

acid for prostate cancer treatment.”
“The expression and function of nicotinic receptor subunits (nAChRs) in the inner ear before the onset of hearing is not well understood. We investigated the mRNA expression of the alpha 9 and alpha 10 nAChR subunits in sensory hair cells of the embryonic and postnatal rat inner ear. We mapped their spatial and temporal expression in cochlear and vestibular hair cells using qPCR, [35S] labeled cRNA in situ hybridization, and alpha-bungarotoxin (alpha-Bgt) to label the presumptive membrane-bound receptor on cochlear hair cells. The results suggest that (1) the mRNA expression of the alpha 9 subunit precedes expression of the alpha 10 subunit in both cochlear and vestibular hair cells, (2) the mRNA expression of both the alpha 9 and alpha buy AZD6244 10 subunits occurs earlier in the vestibular system than in the cochlea, (3) the mRNA expression of both subunits is required for the assembled receptor complexes, and (4) the presumptive assembled receptor, at least in the cochlea, is associated

with synapse formation and the onset of function. CB-839 solubility dmso (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: Prostate cancer cell proliferation is inhibited by 1a,25-dihydroxyvitamin D-3. Survivin is a member of the inhibitors of apoptosis protein family. Several studies indicate that survivin

down-regulation sensitizes human tumor cells of different histological origins to conventional chemotherapeutic drugs. Cyclin-dependent kinase 3 We assessed the effect of survivin gene expression on the proliferation of prostate cancer cells in vitro and in vivo. We also examined the antitumor sensitization effect of survivin inhibition in 1a,25-dihydroxyvitamin D-3 treatment for prostate cancer cells.

Materials and Methods: We knocked down gene expression levels of survivin using siRNA against survivin in vitro and in vivo. We then assessed survivin expression in 1a,25-dihydroxyvitamin D-3 treatment and examined the antitumor sensitization effect of survivin inhibition using siRNA in 1a,25-dihydroxyvitamin D-3 treatment of hormone resistant prostate cancer cells.

Results: In vitro and in vivo siRNA against survivin significantly inhibited cell and tumor growth compared with control siRNA. In LNCaP and PC3 cells 1a,25-dihydroxyvitamin D-3 decreased survivin gene expression and inhibited cell proliferation. However, survivin gene expression and cell proliferation were not inhibited in DU145 cells but after siRNA transfection against survivin DU145 cell proliferation was inhibited by 1a,25-dihydroxyvitamin D-3.

Conclusions: Findings suggest that survivin has a significant association with prostate cancer cell proliferation and an essential role in 1a,25-dihydroxyvitamin D-3 induced prostate cancer cell growth inhibition.