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

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

Primer sequences used for plasmid construction.

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

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

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

miR-182-5p binds to the 3’ UTR of FOXF2, RECK and MTSS1 mRNAs and down-regulates expression.

<p>A. FOXF2, RECK and MTSS1 3’UTR position and complementary miR-182-5p sequence. B. 3’UTR Luciferase assay (miR-NC and miR-182-5p precursor), Error bars represent±S.D. (standard deviation). C. Protein expression of FOXF2, RECK, MTSS1, MMP-2 and beta-tubulin in miR-NC inhibitor or miR-182-5p inhibitor transfected prostate cancer cells (PC-3, DU145).</p

Prostate cancer patient information (n = 52).

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

Effect of RECK and MTSS1 over-expression on prostate cancer cell function.

<p>At 24 hours after transfection of either pCMV6-empty, pCMV6-RECK or pCMV6-MTSS1 into prostate cancer cells (PC-3 and DU 145), RECK and MTSS1 expression levels were verified by real time RT-PCR (A) and Western analysis (B) C. Cell viability assay, D. Invasion assay, E. Wound healing assay, Error bars represent±S.D. (standard deviation).</p