Identification of a tumor-suppressive human-specific microRNA within the FHIT tumor-suppressor gene.

Cancer Res

Authors' Affiliations: Department of Medical Molecular Biology, Beijing Institute of Biotechnology; Center of Computational Biology, Beijing Institute of Basic Medical Sciences; Department of Pathology, Chinese PLA General Hospital; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University; School of Biology, Georgia Institute of Technology, Atlanta, Georgia; Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania; and Genome Institute, National Center for Genetic Engineering and Biotechnology, Pathumthani, Thailand.

Published: April 2014

AI Article Synopsis

  • Loss of the FHIT gene, a tumor suppressor, is linked to worse outcomes in tumors, even though it generally promotes cell death and controls harmful reactive oxygen species.
  • Researchers used various techniques, including bioinformatics and mouse models, to discover a new microRNA from the FHIT gene that could play a role in cancer suppression.
  • This microRNA may help clarify how the Fhit gene functions in human cancers and its potential impact on cancer development.

Article Abstract

Loss or attenuated expression of the tumor-suppressor gene FHIT is associated paradoxically with poor progression of human tumors. Fhit promotes apoptosis and regulates reactive oxygen species; however, the mechanism by which Fhit inhibits tumor growth in animals remains unclear. In this study, we used a multidisciplinary approach based on bioinformatics, small RNA library screening, human tissue analysis, and a xenograft mouse model to identify a novel member of the miR-548 family in the fourth intron of the human FHIT gene. Characterization of this human-specific microRNA illustrates the importance of this class of microRNAs in tumor suppression and may influence interpretation of Fhit action in human cancer.

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Source
http://dx.doi.org/10.1158/0008-5472.CAN-13-3279DOI Listing

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