MicroRNA-210 Regulates Cancer Cell Proliferation through Targeting Fibroblast Growth Factor Receptor-like 1 (FGFRL1)

Department of Nanobio Drug Discovery, Graduate School of Pharmaceutical Sciences, Kyoto University, 46-29 Yoshida Shimoadachi, Sakyo-ku, Kyoto 606-8501, Japan.
Journal of Biological Chemistry (Impact Factor: 4.57). 11/2010; 286(1):420-8. DOI: 10.1074/jbc.M110.170852
Source: PubMed

ABSTRACT The importance of microRNAs (miRNAs) in human malignancies has been well recognized. Here, we report that the expression of microRNA-210 (miR-210) is down-regulated in human esophageal squamous cell carcinoma and derived cell lines. Marked decreases in the level of miR-210 were observed especially in poorly differentiated carcinomas. We found that miR-210 inhibits cancer cell survival and proliferation by inducing cell death and cell cycle arrest in G(1)/G(0) and G(2)/M. Finally, we identified fibroblast growth factor receptor-like 1 (FGFRL1) as a target of miR-210 in esophageal squamous cell carcinoma and demonstrated that FGFRL1 accelerates cancer cell proliferation by preventing cell cycle arrest in G(1)/G(0). Taken together, our findings show an important role for miR-210 as a tumor-suppressive microRNA with effects on cancer cell proliferation.

  • Source
    • "The miR-31 mimics and inhibitors were synthesized at Gene- Pharma (Shanghai, China) and were shown in Table 1. For miR-31 transfections, HiPerFect transfection reagents (Qiagen, Germany) were used for the transfection experiment [23] [24]. The miR-31 mimic or inhibitor (2.0 mL of 20 mM) as well as each negative control were mixed with an equal volume of HiPerFect transfection reagents. "
    [Show abstract] [Hide abstract]
    ABSTRACT: MiR-31 is a critical regulator of gene expression in many pathogenic processes in vertebrates. In this study, we identified p105 as a novel target of miR-31 in Apostichopus japonicus and investigated their regulatory roles in vitro and in vivo. The negative expression profiles between miR-31 and Ajp105 were detected in both LPS-exposed primary coelomocytes and Vibrio splendidus-challenged sea cucumber. Co-infection miR-31 mimics significantly depressed the expression of Ajp105 and increased ROS production in vitro. In contrast, miR-31 inhibitor significantly elevated the expression of Ajp105 and decreased ROS level. Consistently, miR-31 over-expression or Ajp105 silencing in vivo both greatly promoted ROS accumulation. Taken together, our findings confirmed that miR-31 could modulate respiratory burst via targeting Ajp105 during sea cucumber pathological development. Copyright © 2015. Published by Elsevier Ltd.
    Fish &amp Shellfish Immunology 04/2015; 45(2). DOI:10.1016/j.fsi.2015.04.024 · 3.03 Impact Factor
  • Source
    • "miR- 210 was demonstrated to attenuate keratinocyte proliferation and impairs closure in a murine model of ischemic wounds [21]. miR- 210 can also inhibit cancer cell survival and proliferation by inducing cell death and cell cycle arrest in G(1)/G(0) and G(2)/M through targeting fibroblast growth factor receptor-like 1 (FGFRL1) [22]. In the present study, we demonstrated that miR-210 can attenuate LPS-induced inflammatory responses by targeting NF-jB1, indicating miR-210 is also a very important regulator in the immune responses. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Ligation of TLR4 with LPS in macrophages leads to the production of proinflammatory cytokines, which are central to eliminate viral and bacterial infection. However, uncontrolled TLR4 activation may contribute to pathogenesis of inflammatory diseases such as septic shock. In this study, we found microRNA-210 was induced in murine macrophages by LPS. Transfection of miR-210 mimics significantly inhibited LPS-induced production of inflammatory cytokines. In contrast, transfection of anti-miR-210 inhibitors increased LPS-induced expression of proinflammatory cytokines. Furthermore, we demonstrated that miR-210 targets NF-κB1. Therefore, our data identify miR-210 as a very important feedback negative regulator for LPS-induced production of proinflammatory cytokines.
    FEBS letters 04/2012; 586(8):1201-7. DOI:10.1016/j.febslet.2012.03.011 · 3.34 Impact Factor
  • Source
    • "Given the universal regulation of miR-210 by hypoxia, not surprisingly , a variety of miR-210 targets have been identified. Among them are Ephrin A3 [14] [16], RAD52 [17], ACVR1B [18], MNT [19] and FGFRL2 [20]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: E2F family of transcription factors are best known for regulating genes involved in cell cycle control, cell proliferation, tumorigenesis, and apoptosis. Recent evidences have revealed their critical involvement in modulating cellular response to hypoxia and ischemia in a variety of physiological and pathological processes. Of particular interest are findings that E2Fs act as both regulators and targets of microRNAs that govern hypoxic/ischemic angiogenesis. This review focuses on the crosstalk between E2Fs and microRNAs that have been shown to participate in the regulation of angiogenesis, hypoxia response and ischemic disease.
    01/2011; 1(2):110-118.
Show more