Zapi Ace2 Pdf

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asked Jul 30 in History by locustoutput30 (2,670 points)
heterodimerize before binding to their DNA <a href="https://www.ncbi.nlm.nih.gov/pubmed/10773035">Naloxone hydrochloride</a> target site. The AP- proteins are multifunctional and involved in regulating stress response signals, cell growth and apoptosis . Nevertheless, there are data which strongly suggest that c-jun is a growth promoter and proto-oncogene ,. Shemshedini and coworkers showed that, similar to what observed with other AR coactivators, c-jun can mediate AR N-to-C interaction to enhance DNA binding ,. Furthermore, phosphorylated c-jun is frequently overexpressed in human cancers , and has been linked to invasive properties of prostate and breast cancer ,,. However, the role of c-jun activation and possible interaction with AR in the cell fate after exposure to Doc is part of a complex network and remains to be elucidated. This study was carried out to investigate the consequence of interaction of c-jun and AR in taxane treatment of castration resistant prostate cancer cells. To optimize the efficacy of chemotherapy with taxanes we need to identify a specific molecule or pathway which may confer response or resistance. In the   present study we sought to examine the effect of taxanes as single agent or in combination with bicalutamide on AR and its cofactor c-jun in vitro and in vivo. Materials and Methods Cell lines and Reagents The human prostate cancer cell lines LNCaP and PC- were obtained from the American Type Culture Collection ATCC, Manassass, VA. LNb cells were generated in our laboratory from LNCaP cells exposed to bicalutamide ��M in serum reduced to %. Cells were cultured in RPMI LNCaP and Hams-F PC- supplemented with % fetal bovine serum FBS and % penicillin-streptomycin Life Technologies, Paisley, UK. Cells were treated with Docetaxel Taxotere?, Sanofi Aventis and Paclitaxel Paclitaxel?, Actavis, Hafnarfjordeur, Iceland in the concentration stated in each figure. Dihydrotestosterone DHT was purchased from Steraloids Inc. Newport, RI and bicalutamide from AstraZeneca London, UK. All Western blot reagents were purchased from Invitrogen Carlsbad, CA, USA except JNK <a href="http://www.targetmol.com/compound/Naloxone-hydrochloride">Naloxone hydrochloride</a> inhibitor XIV SR Calbiochem, Darmstadt, Germany. Transfection and small interfering RNA siRNA Transient transfections with c-jun, c-jun mutant c-jun Ala/ and AR plasmids all kindly provided by Shao-Yong Chen, Harvard Medical School in PC- prostate cancer cells were performed using FuGENE Roche Diagnostics, Mannheim, Germany as recommended by the manufacturer. The c-jun mutant c-jun Ala/, herein referred as junA, used in experiments carries a mutation at the serine site / Ala/ which is the major target of phophorylation by stress stimuli. For siRNA experiments, PC- and LNCaP cells were transfected for hours with nM siRNA c-jun or non-targeting siRNA Cell Signaling Technology, Danvers, MA, USA. Transfection was performed using X-tremeGENE siRNA transfection reagent Roche Diagnostics according to manufacturers instruction. Proliferation Cell viability was defined by trypan blue exclusion Sigma-Aldrich, St Louis, MO, USA. PC-, LNCaP and LNb cells were seeded in -well plates at a density of , cells per well. After and hours treatment with Doc or DMSO Sigma-Aldrich at the concentrations indicated floating and attached cells were collected by trypsinization. Equal portions of cell suspensions and .% trypan blue were mixed, and the number of viable, trypan blue-excluding cells were counted by using a hemacytometer. The percentage of viable cells was expressed per of the total cells mean �� SD. transfected PC- cells were further evaluated by MTS assay. After hours of transfection cells were exposed to Doc or remained untreated for further hours. After incub

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