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Analysis of receptor mechanisms mediating the induction of MMP-9 expression in THP-1 cells by AFP. Maraviroc, an inhibitor of chemokine receptor CCR5, was added to the cells in the indicated concentrations 1 hour before addition of 50 μg/ml AFP or 150 ng/ml RANTES. After 24 hours of cell stimulation, conditioned media were collected and analyzed for MMP-9 activity by the method of zymography.
Rating
Source
Dr Mikhail Menshikov of Cardiology Research Center. Maraviroc purchased from Selleck
Method
zymography
Cell Lines
THP-1 cells
Concentrations
0-50 μM
Incubation Time
24 h
Results
Analysis of receptor mechanisms mediating the induction of MMP-9 expression in THP-1 cells by AFP.
A,IC50 of Pazopanib that block ANDV-induced EC permeability. Endothelial cells were ANDV infected, and 3 days postinfection the permeability of cells in response to VEGF addition was determined in the presence or absence of increasing amounts of kinase inhibitor. The effect of inhibitors is presented as the percentage of ANDV-induced permeability of inhibitor-treated monolayers 3 days postinfection and 30 min post-VEGF and FITC-dextran addition. B, VEGFR2-Src inhibitors block ANDV-induced permeability. Endothelial cells were plated on vitronectin-coated Transwell inserts and infected at an MOI of 0.5 in triplicate with ANDV. Three days postinfection, the permeability of ANDV- and mock-infected endothelial cell monolayers was determined as described for Fig. 1 at indicated times in the presence or absence of Pazopanib.
Rating
Source
J Virol, 2011, 85, 2296–2303. Pazopanib HCl purchased from Selleck
Method
Endothelial cell permeability assay
Cell Lines
Endothelial cell
Concentrations
0-100 nM
Incubation Time
15-60 min
Results
Figure A defines concentrations of kinase inhibitors which block ANDV-induced EC permeability approximately 50% (IC50s).The IC50s of pazopanib is 100 nM. we assessed the abilities of VEGFR2 and SFK inhibitors to block ANDV-induced permeability at their IC50s from 15 to 60 min after VEGF addition. The VEGFR2 kinase inhibitor pazopanib inhibited ANDV-induced permeability by 40 to 60% at nanomolar IC50 levels (Figure B).
Cooperative Effects of AR and mTOR Inhibition In Vitro and In Vivo (A) In vitro response of Pten null;Ar+ murine (CaP8) and human (LNCaP) prostate cancer cells to AR knockdown (sh-AR) or pharmacological inhibition of AR (MDV3100, 10 mM) with and without rapamycin (R: 1 nM) treatment (Sc, control sh oligo). (B and D) In vivo response to treatments with castration, MDV3100, rapamycin, or their combinations as measured by cell proliferation (Ki67+cells) and (C and D) tumor burden in Pb-Cre+;-PtenL/L and Pb-Cre+;PtenL/L:ArL/Y mutants. Scale bars represent 2 mm (C), 200 mm (D), and 75 mm (D, inset). Error bars represent mean ± SD.
Rating
Source
Cancer Cell, 2011, 19, 1–13. Rapamycin (Sirolimus) purchased from Selleck
Method
Cell viability Analysis
Cell Lines
Ar+murine (CaP8) and human (LNCaP) prostate cancer cells, Pb-Cre+;PtenL/L mice, Pb-Cre+;PtenL/L;ArL/Y mice
Concentrations
1 nM, 4 mg/kg
Incubation Time
0-4 weeks
Results
These data suggest that CaPs with AR loss have greater reliance upon the PI3K/AKT/mTOR-signaling pathways and that combined AR/androgen blockage in conjunction with PI3K/AKT/mTOR inhibition (by Rapamycin) is more effective for CaPs initiated by PTEN loss or PI3K/AKT activation.
