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


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.

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    • "So far, we identified FgfrL1 protein only if the corresponding cDNA was over-expressed in cell culture from a strong CMV promoter [8]. This fact raises doubts about several recent reports, which detected FgfrL1 protein with polyclonal antibodies in mouse kidney [7], rat diaphragm [25], epithelium of human bladder [26] and stroma of esophageal tumors [27]. It is therefore conceivable that commercial polyclonal antibodies cross-react with unrelated proteins. "
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