Formation of 8-epi-prostaglandin F2α by exogenous treatment of C3H 10T1/2 cells with spermine nonoate

<p><b>Copyright information:</b></p><p>Taken from "Enhancement of intracellular γ-tocopherol levels in cytokine-stimulated C3H 10T1/2 fibroblasts: relation to NO synthesis, isoprostane formation, and tocopherol oxidation"</p><p>http://www.biomedcentral.com/1472-6769/7/2</p><p>BMC Chemical Biology 2007;7():2-2.</p><p>Published online 3 Jul 2007</p><p>PMCID:PMC1931582.</p><p></p> Confluent cultures of C3H 10T1/2 cells were treated with either IFN/LPS or PBS at the time of weekly media change. Aqueous spermine nonoate was then added to give the final indicated concentration. After one week, media samples were analyzed for 8-epi-prostaglandin F2α as described in the Methods section. Values are reported as pg/ml 8-epi-prostaglandin F2α ± SEM (n = 6)

Cellular uptake of tocopherols treated with a mixture of tocopherols in medium

<p><b>Copyright information:</b></p><p>Taken from "Enhancement of intracellular γ-tocopherol levels in cytokine-stimulated C3H 10T1/2 fibroblasts: relation to NO synthesis, isoprostane formation, and tocopherol oxidation"</p><p>http://www.biomedcentral.com/1472-6769/7/2</p><p>BMC Chemical Biology 2007;7():2-2.</p><p>Published online 3 Jul 2007</p><p>PMCID:PMC1931582.</p><p></p> Cells were grown to confluence and given a media change followed by tocopherol treatment (Day 0). A second media change and tocopherol re-treatment was performed on Day 7. Tocopherols (α-,γ-; 5.0 μM each in ethanol) were measured in cells in triplicate and cell numbers for each treatment group determined as described under Methods for the extraction and analysis of tocopherols from cells and for cell counting. Data points represent the mean of three determinations ± SEM

miR-182-5p expression and association with clinical parameters in bladder cancer tissues.

<p>A. miR-182-5p expression in clinical samples and bladder cancer cell lines, B. Association of miR-182-5p with clinic-pathological parameters, C. Kaplan Meier plots of overall survival.</p

Effect of miR-182-5p over-expression on bladder cancer cell function (T24, UM-UC-3).

<p> Two bladder cancer cell lines (T24 and UM-UC-3) were transiently transfected with either miR-182-5p precursor or control (miR-NC). A. Relative miR-182-5p expression, B. Cell viability assay, C. Invasion assay, D. Wound healing assay (24 hours), E. Flow cytometric analysis of apoptosis in miR-NC or miR-182-5p transfected BC cells.</p

Primer sequences used for plasmid construction.

<p>Primer sequences used for plasmid construction.</p

miR-182-5p binds to the 3′ UTR of RECK and Smad4 mRNAs and down-regulates expression.

<p>A. RECK and Smad4 3′UTR position and complementary miR-182-5p sequences. B. 3′UTR Luciferase assay (miR-NC and miR-182-5p precursor), C. RECK, Smad4 and beta-tubulin protein expression in miR-NC inhibitor or miR-182-5p inhibitor transfected bladder cancer cells (T24, UM-UC-3).</p

Effect of miR-182-5p knock down on prostate cancer cells (PC-3, DU145).

<p>Two prostate cancer cell lines (PC-3 and DU145) were transiently transfected with either miR-182-5p inhibitor or miR-negative control (miR-NC-inhibitor). A. Relative miR-182-5p expression (miR-NC inhibitor or miR-182-5p inhibitor transfected PC cells), B. Cell viability assay (miR-NC inhibitor or miR-182-5p inhibitor transfected PC cells), C. Invasion assay, D. Wound healing assay (24 hours). Error bars represent±S.D. (standard deviation).</p

Inhibition of <i>in vivo</i> tumor growth by miR-182-5p knockdown in PC3 cells.

<p>A. Time record of tumor size in miR-NC and miR-182-5p inhibitor xenografts. B. Relative miR-182-5p expression at injection of cells and harvest of xenografts. Error bars represent ±S.D. (standard deviation). MiR-182-5p expression was significantly lower in the miR-182-5p inhibitor group. C. Typical gross appearance of nude mouse tumors in control and miR-182-5p inhibitor groups. D. Expression of FOXF2, RECK and MTSS1 protein in tumor xenografts.</p

Expression of miR-182-5p in cell lines and effect of miR-182-5p overexpression on normal prostate cells (RWPE-1).

<p>A. The expression of miR-182-5p was significantly higher in three prostate cancer cell lines compared to a normal prostate cell line (RWPE-1), B. Relative miR-182-5p expression (miR-NC or miR-182-5p precursor transfected RWPE-1 cells), B. cell viability assay (miR-NC or miR-182-5p precursor transfected RWPE-1 cells), C. Wound healing assay (miR-NC or miR-182-5p precursor transfected RWPE-1 cells). Error bars represent ±S.D. (standard deviation).</p

Prostate cancer patient information (n = 52).

<p>Prostate cancer patient information (n = 52).</p