Purpose Breast cancer is the most frequently diagnosed malignancy in women worldwide. MicroRNAs (miRNAs) are thought to serve as potential biomarkers in various cancers, including breast cancer. Methods We evaluated the miRNA expression profiles in 1,083 breast cancer samples and 104 normal breast tissues from The Cancer Genome Atlas database. We used the edgeR package of R software to analyze the differentially expressed miRNAs in normal and cancer tissues, and screened survival-related miRNAs by Kaplan-Meier analysis. A receiver operating characteristic curve was generated to evaluate the accuracy of these miRNAs as molecular markers for breast cancer diagnosis. Furthermore, the functional role of these miRNAs was verified using cell experiments. Targets of candidate miRNAs were predicted using 9 online databases, and Gene Ontology (GO) functional annotation and pathway analyses were conducted using Database for Annotation, Visualization and Integrated Discovery online tool. Results A total of 68 miRNAs showed significantly different expression patterns between the groups ( p < 0.001), and 13 of these miRNAs were significantly associated with poor survival ( p < 0.05). Three miRNAs with high specificity and sensitivity, namely, miR-148b-3p, miR-190b, and miR-429, were selected. In vitro experiments showed that the overexpression of these 3 miRNAs significantly promoted the proliferation and migration of MDA-MB-468 and T47D cells and reduced the apoptosis of T47D cells. GO and pathway enrichment analyses revealed that the targets of these dysregulated miRNAs were involved in many critical cancer-related biological processes and pathways. Conclusion The miR-148b-3p, miR-190b, and miR-429 may serve as potential diagnostic and prognostic markers for breast cancer. This study demonstrated the roles of these 3 miRNAs in the initiation and progression of breast cancer.
Hepatocellular carcinoma (HCC) is the most common cancer type. There is a correlation between selenium (Se) deficiency and the incidence of HCC. To clarify the effects of Se level on the risk of HCC patients, a meta-analysis was performed. A total of 9 articles published between 1994 and 2016 worldwide were selected through searching PubMed, EMBASE, web of science, Cochrane Library, Springer Link, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biology Medicine (CBM), and the information were analyzed using a meta-analysis method. Heterogeneity was assessed by using the I2 index. Publication bias was evaluated by Begg's Test analysis. Pooled analysis indicated that patients with HCC had lower Se levels than the healthy controls [standardized mean difference (SMD)= −1.08, 95% confidence intercal (CI) = (−0.136, −0.08), P < 0.001]. Further subgroup analysis showed this effect to be independent of the study design, race or sample collection. In conclusion, this meta-analysis suggested an inverse correlation between Se level and the risk of HCC in humans patients.
MicroRNAs (miRNAs) are small, non-coding RNAs that can serve as tumor suppressor genes or oncogenes in tumorigenesis. More and more evidence demonstrate that abnormal expression of miRNAs lead to the gastric carcinoma occurrence. In the present study, we revealed that the expression levels of miR-520f were significantly down-regulated in gastric carcinoma cells and clinical gastric carcinoma samples. Next, we demonstrated that introduction of miR-520f inhibited the growth of gastric carcinoma cells in vitro. However, down-regulate the expression levels of miR-520f by anti-miR-520f lead to an enhanced cell proliferation, implying that miR-520f maybe serve as a novel tumor suppressor. Moreover, we found that ATPase family AAA domain-containing protein 2 (ATAD2) was one target genes of miR-520f downstream regulator, which caused the decreased expression of ATAD2. Meanwhile, the overexpression of ATAD2 reversed the inhibited proliferation ability caused by miR-520f. Therefore, our find that miR-520f involves in gastric carcinoma proliferation, pointing a therapeutic probability of miR-520f in the therapy of gastric carcinoma.
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