Comparisons of computation cost and aggregate signature size.

<p>Comparisons of computation cost and aggregate signature size.</p

Bland-Altman plots of inter-observer reproducibility of the NASCET and WASID methods.

<p>(A, C and E) WASID method for Observers 1&2, 1&3 and 2&3, respectively. (B, D and F) NASCET method for Observers 1&2, 1&3 and 2&3, respectively.</p

Scatterplots of NASCET and WASID measurements.

<p>(A) The measurements of Observer 1. (B) The measurements of Observer 2. (C) The measurements of Observer 3. (D) The mean measurements of all 3 observers.</p

Bland-Altman plots of intra-observer reproducibility of the NASCET and WASID methods.

<p>(A, C and E) WASID method for Observer 1, 2 and 3, respectively. (B, D and F) NASCET method for Observer 1, 2 and 3, respectively.</p

Additional file 4: of Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer

The expression of RhoA and miR-125a-3p in GSE32688. (XLSX 11 kb

Additional file 3: of Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer

NORAD expression among 8 cell lines. (TIFF 728 kb

Additional file 2: of Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer

Primers used for qRT-PCR assays. (XLSX 9 kb

Additional file 1: of Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer

Box plots of GSE15471 and GSE16515. (TIFF 154 kb

miR-150-5p Inhibits Hepatoma Cell Migration and Invasion by Targeting MMP14

<div><p>Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide. Despite progress in diagnostics and treatment of HCC, its prognosis remains poor because the molecular mechanisms underlying hepatocarcinogenesis are not well understood. In the study, we focused on identifying the role of miRNAs in HCC progression. miRNA microarray was used to analyze the differentially expressed miRNAs, and the results were validated by qPCR. We found that the miR-150-5p expression is down-regulated in HCC tissues compared with pair non-tumor tissues. miR-150-5p expression is also decreased in metastatic cancer tissues compared with pair primary tissues, indicating that miR-150-5p may be involved in HCC metastasis. Functionally, miR-150-5p inhibition significantly promotes hepatoma cell migration and invasion, whereas miR-150-5p overexpression suppresses cancer cell migration and invasion <i>in</i><i>vitro</i>. The matrix metalloproteinase 14 (MMP14) is identified as a new target gene of miR-150-5p. miR-150-5p markedly inhibits MMP14 expression in hepatoma cells, and miR-150-5p expression is negative correlation with MMP14 expression <i>in</i><i>vivo</i>. More important, re-expression of MMP14 in hepatoma cells partially reverses the effect of miR-150-5p in inhibiting cell invasion.</p></div

The characteristics of patients with HCC.

<p>Cell invasion assay of Huh7 cells (A) or HepG2 cells (B) after miR-150-5p overexpression or miR-150-5p plus MMP14 overexpression. Data are shown as the mean ± SD based on at least three independent experiments (C). *<i>p</i><0.05.</p><p>The characteristics of patients with HCC.</p