Meta-analysis results of complication incidence.

<p>Meta-analysis results of complication incidence.</p

Meta-analysis results.

a<p>Random-effects model.</p

Meta-analysis results of patient survival rate.

<p>Meta-analysis results of patient survival rate.</p

Egger test results of studies on complication incidence.

<p>Egger test results of studies on complication incidence.</p

Flow of included studies.

<p>Flow of included studies.</p

Meta-analysis results of graft survival rate.

<p>Meta-analysis results of graft survival rate.</p

Egger test results of studies on patient survival rate.

<p>Egger test results of studies on patient survival rate.</p

MiR-30c functions as a tumour suppressor through the miR-30c-MTA-1 signalling pathway.

<p>(A). A MTT assay shows the cell viability (left) and relative cell proliferation (right) were repressed by transfection of siR-MTA-1 at 72 and 96 h. (B). Representative photographs of the wound-healing assay show the migratory ability of the transfected cells at 0, 24 and 48 h after wounding. (C). Representative photographs of cell invasion in a transwell assay. The average number of cells was counted from 5 random microscopic fields (×200). The values shown are the mean values ± SD of relative cell invasion. (D) and (E). Cotransfection of miR-30c-inhibitor and siR-MTA-1; cotransfection of miR-30c-inhibitor and siR-sc served as the control. (D). Compared with the control transfection, cell viability (upper) and relative cell proliferation (lower) was suppressed at 96 h. (E). Representative photographs of cell invasion in a transwell assay. The average number of cells was counted from 5 random microscopic fields (×200). The values shown are the mean values ± SD of relative cell invasion. The differences of relative cell proliferation between the groups appeared at 96 h after transfection. (*P<0.05, **P<0.01).</p

Estrogen regulates the expression of miR-30c in EC cells.

<p>(A). MiR-30c was decreased upon treatment with 10⁻⁸ M and 10⁻¹⁰ M E₂ at 6, 12, 24 and 48 h after treatment by qRT-PCR analysis in Ishikawa cells. The treatment with 10⁻⁸ M E₂ exerted a more significant inhibition except at 48 h. (B). 10⁻⁸ M ICI182780 partially reversed the reduction of miR-30c levels induced by the treatment with 10⁻⁸ M and 10⁻¹⁰ M E₂ at 24 h after cotreatment in Ishikawa cells. (C). Pre-miR-30c levels were reduced by E₂ treatment in both the Ishikawa and HEC-1-B cells (upper). Pri-miR-30c levels were reduced by E₂ treatment in Ishikawa but not in HEC-1-B cells (lower). (D). MiR-30c levels were reduced upon 10⁻⁸ M and 10⁻¹⁰ M E₂ treatment at 6, 12, 24 and 48 h after treatment by qRT-PCR analysis in HEC-1-B cells. The effect of the two concentrations differed at 12 h after treatment. (E). 10^-8 M ICI182780 did not reverse reduction of miR-30c levels induced by the treatment with 10⁻⁸ M and 10⁻¹⁰ M E₂ at 48 h after cotreatment in HEC-1-B cells. (F). Treatment with 10⁻⁸ M E₂ up-regulated mRNA expression of MTA-1 in both the Ishikawa cells and HEC-1 cells at 24 and 48 h, respectively, an effect that was reversed by cotreatment with 10⁻⁸ M ICI182780 in the Ishikawa cells (upper) but not the HEC-1-B cells ((lower). (*P<0.05, **P<0.01).</p

MiR-30c regulates cell proliferation, migration and invasion in EC.

<p>(A). A MTT assay shows that miR-30c mimics suppressed cell viability (upper), whereas miR-30c inhibitor promoted cell viability (lower). (B). MiR-30c-mimics reduces relative cell proliferation (upper), whereas miR-30c-inhibitor increases relative cell proliferation (lower), respectively at 72 and 96 h after transfection. (C). Representative photographs of the wound-healing assay showing the migratory ability of the transfected cells at 0, 24 and 48 h after wounding. (D). Representative photographs of cell invasion in a transwell assay. The average number of cells was counted from 5 random microscopic fields (×200). The values shown are the mean values ± SD of relative cell invasion. (*P<0.05, **P<0.01).</p