71 research outputs found

    The Association between Two MicroRNA Variants (miR-499, miR-149) and Gastrointestinal Cancer Risk: A Meta-Analysis

    Get PDF
    <div><p>Background</p><p>MicroRNAs (miRNAs) are small RNA molecules that regulate the expression of corresponding messenger RNAs (mRNAs). Single nucleotide polymorphisms (SNPs) in miRNAs may contribute to cancer susceptibility due to changes in the microRNA’s properties and/or maturation. The present study aimed to investigate the association between two miRNA polymorphisms (miR-499 rs3746444 and miR-149 rs2292832) and gastrointestinal (GI) cancer risk. </p><p>Methodology/Principal Findings</p><p>We conducted a search of case-control studies in PubMed, Wiley Online Library, Web of Science and the CNKI database. Eleven rs3746444 studies and six rs2292832 studies were included in our meta-analysis. The only obvious association between the miR-499 polymorphism and colorectal cancer susceptibility was found in the homozygote comparison (GG vs. AA: OR = 1.66, 95% CI: 1.02–2.70, <i>P</i><sub>h</sub> = 0.10, <i>P</i> = 0.04). No significant association was found in the subgroup analysis for ethnicity and risk of hepatocellular and gastric cancer. A marginally elevated GI cancer risk was discovered in the recessive model for miR-149 (TT vs. TC+CC: OR = 1.15, 95% CI: 1.03–1.30, <i>P</i><sub>h</sub> = 0.68, <i>P</i> = 0.02). Stratifying the results by ethnicity revealed a slight association between the recessive model and the Asian population (TT vs. TC+CC: OR = 1.14, 95% CI: 1.01–1.29, <i>P</i><sub>h</sub> = 0.79, <i>P</i> = 0.03).</p><p>Conclusions/Significance</p><p>The present meta-analysis indicates that miR-499 may be associated with the risk to colorectal cancer. MiR-149 may confer a marginally increased risk of susceptibility to gastrointestinal cancer, especially for Asians. </p></div

    Meta-analysis of miR-499 and miR-149 with gastrointestinal cancer susceptibility.

    No full text
    <p>Meta-analysis of miR-499 and miR-149 with gastrointestinal cancer susceptibility.</p

    A: Forest plot of cancer risk associated with miR-149 (TT vs TC+CC) in different types of cancers.

    No full text
    <p><b>B</b>: <b>Forest plot of cancer risk associated with miR-149 (TT vs TC+CC) in different ethnicity</b>. </p

    The Results of Meta-regression of rs3746444 (P).

    No full text
    <p>The Results of Meta-regression of rs3746444 (P).</p

    Tumorigenicity of the ALDH<sup>high</sup> and ALDH<sup>low</sup> H460 cells.

    No full text
    <p>An equal number of ALDH<sup>high</sup> and ALDH<sup>low</sup> cells were inoculated into the opposite flanks of the same individuals. The sizes of the tumors were measured 3 times per week. (A) The tumor sizes of mice subjected to ALDH<sup>high</sup> H460 cells were much more larger than the ALDH<sup>low</sup> H460 cells. (B–C) show the representative tumor growth curves from 3 different mice.</p

    ALDH<sup>high</sup>-CD8+ T treatment prolongs the overall survival of the tumor-bearing mice.

    No full text
    <p>The mice treated with ALDH<sup>high</sup>-CD8+ T cells survived much longer than the mice treated with PBS, H-CD8+ T, or ALDH<sup>low</sup>-CD8+ T cells.</p

    The identification of ALDH<sup>high</sup> cells from the human non-small cell lung cancer cells and primary tumor cells.

    No full text
    <p>ALDEFLUOR was used as a single marker to identify the ALDH<sup>high</sup> cells from the H460 cell line (A) and freshly harvested tumor cells (B). Tumor cells incubated with both ALDH and DEAB were used as a negative control.</p
    corecore