MicroRNA-155, induced by FOXP3 through transcriptional repression of BRCA1 , is associated with tumor initiation in human breast cancer MicroRNA-155, induced by FOXP3 through transcriptional repression of BRCA1, is associated with tumor initiation in human breast cancer

Background: Numerous studies have shown that miRNA levels are closely related to the survival time of patients with colon, rectal, or colorectal cancer (CRC). However, the outcomes of different investigations have been inconsistent. Accordingly, a meta-analysis was conducted to study associations among the three types of cancers. Materials and methods: Studies published in English that estimated the expression levels of miRNAs with survival curves in CRC were identified until May 20, 2017 by online searches in PubMed, Embase, Web of Science, and the Cochrane Library by two independent authors. Pooled HRs with 95% CIs were used to estimate the correlation between miRNA expression and overall survival. Results: A total of 63 relevant articles regarding 13 different miRNAs, with 10,254 patients were ultimately included. CRC patients with high expression of blood miR141 (HR 2.52, 95% CI 1.68–3.77), tissue miR21 (HR 1.31, 95% CI 1.12–1.53), miR181a (HR 1.52, 95% CI 1.26–1.83), or miR224 (HR 2.12, 95% CI 1.04–4.34), or low expression of tissue miR126 (HR 1.55, 95% CI 1.24–1.93) had significantly poor overall survival (P<0.05). Conclusion: In general, blood miR141 and tissue miR21, miR181a, miR224, and miR126 had significant prognostic value. Among these, blood miR141 and tissue miR224 were strong biomarkers of prognosis for CRC.

Prostate cancer (PC) is known as the most common cancer and is ranked second in cancer-related deaths in males. Accumulating evidence implicates microRNAs (miRNAs) may play key roles in tumorigenesis. We investigated the effects of microRNA-1 (miR-1) on the viability and proliferation of prostate cancer cells and the underlying mechanism. We first detected the miR-1 expression level in the PC cells by quantitative real-time PCR (qRT-PCR). The relation between the level of miR-1 and c-Met was investigated via luciferase reporter assay. Cell viability and proliferation were analyzed via MTT assay and flow cytometry in PC cells. Western blot was used for examining the related signaling pathway. MiR-1 expression was decreased and c-Met expression was increased in PC cells. Subsequently, we found that overexpression of miR-1 could inhibit viability and proliferation of PC cells functionally. Furthermore, the dual luciferase reporter assay results indicated that the c-Met is the target gene of miR-1. Western blot results indicated that this inhibition on the viability and proliferation of PC cells was via regulation of c-Met/AKT/mTOR signaling pathway. In conclusion, this study provides novel insight into the role of miR-1 in PC, and the results demonstrated that miR-1 could inhibit viability and proliferation of PC cells by targeting the c-Met/Akt/mTOR signaling pathway. MiR-1 might be a potential candidate for application in the treatment of PC.