Cited by 5,697MicroRNA in disease regulationCancer-related molecular mechanisms researchPlant Molecular Biology Research

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A microRNA expression signature of human solid tumors defines cancer gene targets

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Abstract

Small noncoding microRNAs (miRNAs) can contribute to cancer development and progression and are differentially expressed in normal tissues and cancers. From a large-scale miRnome analysis on 540 samples including lung, breast, stomach, prostate, colon, and pancreatic tumors, we identified a solid cancer miRNA signature composed by a large portion of overexpressed miRNAs. Among these miRNAs are some with well characterized cancer association, such as miR-17-5p , miR-20a , miR-21 , miR-92 , miR-106a , and miR-155 . The predicted targets for the differentially expressed miRNAs are significantly enriched for protein-coding tumor suppressors and oncogenes ( P < 0.0001). A number of the predicted targets, including the tumor suppressors RB1 (Retinoblastoma 1) and TGFBR2 (transforming growth factor, beta receptor II) genes were confirmed experimentally. Our results indicate that miRNAs are extensively involved in cancer pathogenesis of solid tumors and support their function as either dominant or recessive cancer genes.

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Crossref · 10.1073/pnas.0510565103

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  • miR-21 is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins.

    “Substantial data indicate that microRNA 21 (miR-21) is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins.”
  • miR-21 expression is highly upregulated in a variety of solid tumors, including GBM, breast, lung, colon, prostate, pancreas, and stomach cancers.

    “Its expression is highly upregulated in a variety of solid tumors, including GBM, breast, lung, colon, prostate, pancreas, and stomach cancers (5, 54).”
  • A large scale survey of 540 tumor samples revealed miR-21 was the only miRNA up-regulated in all these tumors.

    “A large scale survey to determine the miRNA signature of 540 tumor samples including lung, breast, stomach, prostate, colon, and pancreatic tumors and their respective normal adjacent tissue revealed miR-21 was the only miRNA up-regulated in all these tumors (Volinia et al., 2006).”

    From Modulation of K-Ras-Dependent Lung Tumorigenesis by MicroRNA-21 (2010) · cites this paper as Volinia et al., 2006

  • miR-21 is up-regulated in the majority of human cancers profiled to date.

    “The majority of these profiling studies have reported increased levels of miR-21 in most human cancers (6,(8)(9)(10).”

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Research works printed but not linked: 29

  1. V. Ambros Cell 113, 673–676 (2003). · DOI
  2. B. R. Cullen Mol. Cell 16, 861–865 (2004). · DOI
  3. D. P. Bartel Cell 116, 281–297 (2004). · DOI
  4. G. A. Calin, C. D. Dumitru, M. Shimizu, R. Bichi, S. Zupo, E. Noch, H. Aldler, S. Rattan, M. Keating, K. Rai, et al. Proc. Natl. Acad. Sci. USA 99, 15524–15529 (2002). · DOI · Paper page
  5. M. Z. Michael, O. C. SM, N. G. van Holst Pellekaan, G. P. Young, R. J. James Mol. Cancer Res 1, 882–891 (2003).
  6. M. Metzler, M. Wilda, K. Busch, S. Viehmann, A. Borkhardt Genes Chromosomes Cancer 39, 167–169 (2004). · DOI
  7. J. Takamizawa, H. Konishi, K. Yanagisawa, S. Tomida, H. Osada, H. Endoh, T. Harano, Y. Yatabe, M. Nagino, Y. Nimura, et al. Cancer Res 64, 3753–3756 (2004). · DOI
  8. P. S. Eis, W. Tam, L. Sun, A. Chadburn, Z. Li, M. F. Gomez, E. Lund, J. E. Dahlberg Proc. Natl. Acad. Sci. USA 102, 3627–3632 (2005). · DOI
  9. J. A. Chan, A. M. Krichevsky, K. S. Kosik Cancer Res 65, 6029–6033 (2005). · DOI · Paper page
  10. J. Kluiver, S. Poppema, D. de Jong, T. Blokzijl, G. Harms, S. Jacobs, B. J. Kroesen, A. van den Berg J. Pathol 207, 243–249 (2005). · DOI
  11. C. M. Croce, G. A. Calin Cell 122, 6–7 (2005). · DOI
  12. L. He, J. M. Thomson, M. T. Hemann, E. Hernando-Monge, D. Mu, S. Goodson, S. Powers, C. Cordon-Cardo, S. W. Lowe, G. J. Hannon, S. M. Hammond Nature 435, 828–833 (2005). · DOI
  13. K. A. O’Donnell, E. A. Wentzel, K. I. Zeller, C. V. Dang, J. T. Mendell Nature 435, 839–843 (2005). · DOI
  14. C.-G. Liu, G. A. Calin, B. Meloon, N. Gamliel, C. Sevignani, M. Ferracin, D. C. Dumitru, M. Shimizu, S. Zupo, M. Dono, et al. Proc. Natl. Acad. Sci. USA 101, 9740–9744 (2004). · DOI · Paper page
  15. J. Lu, G. Getz, E. A. Miska, E. Alvarez-Saavedra, J. Lamb, D. Peck, A. Sweet-Cordero, B. L. Ebert, R. H. Mak, A. A. Ferrando, et al. Nature 435, 834–838 (2005). · DOI
  16. G. A. Calin, C. G. Liu, C. Sevignani, M. Ferracin, N. Felli, C. D. Dumitru, M. Shimizu, A. Cimmino, S. Zupo, M. Dono, et al. Proc. Natl. Acad. Sci. USA 101, 11755–11760 (2004). · DOI
  17. G. A. Calin, M. Ferracin, A. Cimmino, G. Di Leva, M. Shimizu, S. Wojcik, M. V. Iorio, R. Visone, N. I. Sever, M. Fabbri, et al. N. Engl. J. Med 353, 1793–1801 (2005). · DOI
  18. M. V. Iorio, M. Ferracin, C. G. Liu, A. Veronese, R. Spizzo, S. Sabbioni, E. Magri, M. Pedriali, M. Fabbri, M. Campiglio, et al. Cancer Res 65, 7065–7070 (2005). · DOI · Paper page
  19. S. H. Jung, H. Bang, S. Young Biostatistics 6, 157–169 (2005). · DOI
  20. B. P. Lewis, C. B. Burge, D. P. Bartel Cell 120, 15–20 (2005). · DOI · Paper page
  21. A. A. Ali, J. N. Marcus, J. P. Harvey, R. Roll, C. P. Hodgson, D. M. Wildrick, A. Chakraborty, B. M. Boman FASEB J 7, 931–937 (1993). · DOI
  22. M. B. Buck, P. Fritz, J. Dippon, G. Zugmaier, C. Knabbe Clin. Cancer Res 10, 491–498 (2004). · DOI
  23. G. Anumanthan, S. K. Halder, H. Osada, T. Takahashi, P. P. Massion, D. P. Carbone, P. K. Datta Br. J. Cancer 93, 1157–1167 (2005). · DOI
  24. N. Yanaihara, N. Caplen, E. Bowman, M. Seike, K. Kumamoto, M. Yi, R. M. Stephens, A. Okamoto, J. Yokota, T. Tanaka, et al. Cancer Cell, in press. (2006).
  25. S. M. Johnson, H. Grosshans, J. Shingara, M. Byrom, R. Jarvis, A. Cheng, E. Labourier, K. L. Reinert, D. Brown, F. J. Slack Cell 120, 635–647 (2005). · DOI
  26. A. Cimmino, G. A. Calin, M. Fabbri, M. V. Iorio, M. Ferracin, M. Shimizu, S. E. Wojcik, R. I. Aqeilan, S. Zupo, M. Dono, et al. Proc. Natl. Acad. Sci. USA 102, 13944–13949 (2005). · DOI
  27. S. Griffiths-Jones Nucleic Acids Res 32, D109–D111 (2004). · DOI
  28. V. G. Tusher, R. Tibshirani, G. Chu Proc. Natl. Acad. Sci. USA 98, 5116–5121 (2001). · DOI · Paper page
  29. R. Tibshirani, T. Hastie, B. Narasimhan, G. Chu Proc. Natl. Acad. Sci. USA 99, 6567–6572 (2002). · DOI

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Metadata

Authors
Volinia, S., Calin, G. A., Liu, C.-G., Ambs, S., Cimmino, A., Petrocca, F., Visone, R., Iorio, M., Roldo, C., Ferracin, M., Prueitt, R. L., Yanaihara, N., Lanza, G., Scarpa, A., Vecchione, A., Negrini, M., Harris, C. C., & Croce, C. M.
Affiliations
  • The Ohio State University (US)
  • National Institutes of Health (US)
  • University of Ferrara (IT)
  • University of Verona (IT)
  • Azienda Ospedaliera Sant'Andrea (IT)
Venue
Proceedings of the National Academy of Sciences
Published
2006-02-03
Volume
103
Issue
7
Pages
2257-2261
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2135810600
Cited by
5,697
References
0
Citations by year
2026: 53 · 2025: 77 · 2024: 95 · 2023: 173 · 2022: 159 · 2021: 180 · 2020: 220 · 2019: 215 · 2018: 284 · 2017: 379 · 2016: 339 · 2015: 439 · 2014: 445 · 2013: 482 · 2012: 490
FWCI
106.28
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed (publishedVersion)
  • Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
  • Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
Funders
  • National Institutes of Health (4p01ca081534-16)
  • National Cancer Institute (P01 CA81534, P01CA076259, P30CA056036, P01-CA-081534)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Plant Molecular Biology Research
Keywords
microRNA signature, solid tumors, miRNA target genes, miR-17-5p, miR-21, miR-106a, miR-155, miR-92, miR-20a, tumor suppressor, oncogenes, RB1, TGFBR2, microRNA overexpression, lung cancer, breast cancer, gastric cancer, prostate cancer, colon cancer, pancreatic cancer
MeSH terms
Humans, Neoplasms, Tumor Cells, Cultured, Genes, Tumor Suppressor, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, MicroRNAs, Genes, Neoplasm

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