Overexpression of miR-200c affects cell migration.

<p><b>(A)</b> After 36 or 48h of transfection with pre-miRNAs in the NSCLC cell lines, cell migration was measured by <i>in vitro</i> scratch assay. High levels of miR-200c reduced cell migration in comparison with control in all cell lines (H23, p = 0.005; A-549, p = 0.0085; HCC-44, p = 0.013), while high levels of miR-141 reduced cell migration only in A-549 (p = 0.04). <b>(B)</b> E-cadherin levels were evaluated by immunohistochemistry and increased levels were observed in cells transfected with pre-miR-200c in comparison with those transfected with pre-miR-141 or pre-miR-control in all three cell lines.</p

OS analysis in the entire cohort.

<p>OS according to <b>(A)</b> miR-200c expression levels in the entire cohort (N = 155); <b>(B)</b> miR-200c expression levels in stage I patients (N = 94); and <b>(C)</b> miR-141 expression levels in stage I patients (N = 94).</p

Main patient characteristics.

<p>Main patient characteristics.</p

OS in 73 patients with adenocarcinoma according to the miR-141/miR-200c risk score.

<p>OS in 73 patients with adenocarcinoma according to the miR-141/miR-200c risk score.</p

Multivariate analysis for OS in the entire cohort (N = 155) and in the subgroup of patients with adenocarcinoma (N = 73).

<p>Multivariate analysis for OS in the entire cohort (N = 155) and in the subgroup of patients with adenocarcinoma (N = 73).</p

Additional file 1: Figure S1. of NKX2–1 expression as a prognostic marker in early-stage non-small-cell lung cancer

NKX2–1 expression according to TTF-1 immunohistochemistry. Figure S2. Kaplan Meier analysis of disease-free survival according to NKX2–1 expression levels in (A) the entire cohort and (B) patients with stage I disease. Figure S3. Kaplan Meier analysis of overall survival according to miR-365 expression levels in (A) the entire cohort and (B) patients harboring neither TP53 nor KRAS mutations. Figure S4. Kaplan Meier analysis of overall survival according to NKX2–1 expression levels in (A) patients with wild-type TP53, (B) patients with TP53 mutations, (C) patients with wild-type KRAS, and (D) patients with KRAS mutations. Figure S5. Kaplan Meier analysis of the impact of NKX2–1 in overall survival in stage I disease (A) WT TP53 patients, (B) TP53 mutated patients, (C) KRAS WT patients, and (D) KRAS mutated patients. (PDF 276 kb