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Transcribed ultraconserved region 339 promotes carcinogenesis by modulating tumor suppressor microRNAs

Author

Listed:
  • Ivan Vannini

    (IRCCS, Gene Therapy Unit)

  • Petra M. Wise

    (Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Children’s Center for Cancer and Blood Diseases and The Saban Research Institute, Children’s Hospital Los Angeles)

  • Kishore B. Challagundla

    (University of Nebraska Medical Center)

  • Meropi Plousiou

    (IRCCS, Gene Therapy Unit)

  • Mirco Raffini

    (IRCCS, Gene Therapy Unit)

  • Erika Bandini

    (IRCCS, Gene Therapy Unit)

  • Francesca Fanini

    (IRCCS, Gene Therapy Unit)

  • Giorgia Paliaga

    (IRCCS, Gene Therapy Unit)

  • Melissa Crawford

    (The Ohio State University)

  • Manuela Ferracin

    (Diagnostic and Specialty Medicine—DIMES, University of Bologna)

  • Cristina Ivan

    (The University of Texas MD Anderson Cancer Center
    The University of Texas MD Anderson Cancer Center)

  • Linda Fabris

    (The University of Texas MD Anderson Cancer Center)

  • Ramana V. Davuluri

    (Northwestern University-Feinberg School of Medicine)

  • Zhiyi Guo

    (The University of Texas MD Anderson Cancer Center)

  • Maria Angelica Cortez

    (The University of Texas MD Anderson Cancer Center
    The University of Texas MD Anderson Cancer Center)

  • Xinna Zhang

    (The University of Texas MD Anderson Cancer Center
    The University of Texas MD Anderson Cancer Center)

  • Lu Chen

    (The University of Texas MD Anderson Cancer Center)

  • Shuxing Zhang

    (The University of Texas MD Anderson Cancer Center)

  • Cecilia Fernandez-Cymering

    (Immunology and Medical Genetics, Comprehensive Cancer Center, Ohio State University)

  • Leng Han

    (McGovern Medical School, The University of Texas Health Science Center at Houston)

  • Silvia Carloni

    (IRCCS, Biosciences Laboratory Unit)

  • Samanta Salvi

    (IRCCS, Biosciences Laboratory Unit)

  • Hui Ling

    (The University of Texas MD Anderson Cancer Center)

  • Mariam Murtadha

    (Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Children’s Center for Cancer and Blood Diseases and The Saban Research Institute, Children’s Hospital Los Angeles)

  • Paolo Neviani

    (Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Children’s Center for Cancer and Blood Diseases and The Saban Research Institute, Children’s Hospital Los Angeles)

  • Barbara J. Gitlitz

    (Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California)

  • Ite A. Laird-Offringa

    (Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California)

  • Patrick Nana-Sinkam

    (Virginia Commonwealth University)

  • Massimo Negrini

    (Surgery and Experimental Medicine and Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara)

  • Han Liang

    (The University of Texas MD Anderson Cancer Center)

  • Dino Amadori

    (Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) S.r.l., IRCCS)

  • Amelia Cimmino

    (National Research Council)

  • George A. Calin

    (The University of Texas MD Anderson Cancer Center
    The University of Texas MD Anderson Cancer Center)

  • Muller Fabbri

    (Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Children’s Center for Cancer and Blood Diseases and The Saban Research Institute, Children’s Hospital Los Angeles)

Abstract

The transcribed ultraconserved regions (T-UCRs) encode long non-coding RNAs implicated in human carcinogenesis. Their mechanisms of action and the factors regulating their expression in cancers are poorly understood. Here we show that high expression of uc.339 correlates with lower survival in 210 non-small cell lung cancer (NSCLC) patients. We provide evidence from cell lines and primary samples that TP53 directly regulates uc.339. We find that transcribed uc.339 is upregulated in archival NSCLC samples, functioning as a decoy RNA for miR-339-3p, -663b-3p, and -95-5p. As a result, Cyclin E2, a direct target of all these microRNAs is upregulated, promoting cancer growth and migration. Finally, we find that modulation of uc.339 affects microRNA expression. However, overexpression or downregulation of these microRNAs causes no significant variations in uc.339 levels, suggesting a type of interaction for uc.339 that we call “entrapping”. Our results support a key role for uc.339 in lung cancer.

Suggested Citation

  • Ivan Vannini & Petra M. Wise & Kishore B. Challagundla & Meropi Plousiou & Mirco Raffini & Erika Bandini & Francesca Fanini & Giorgia Paliaga & Melissa Crawford & Manuela Ferracin & Cristina Ivan & Li, 2017. "Transcribed ultraconserved region 339 promotes carcinogenesis by modulating tumor suppressor microRNAs," Nature Communications, Nature, vol. 8(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01562-9
    DOI: 10.1038/s41467-017-01562-9
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