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Ke S, Li RC, Lu J, et al. MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2. Int J Hematol. 2017;106(2):258-265doi: 10.1007/s12185-017-2232-2.
Ke, S., Li, R. C., Lu, J., Meng, F. K., Feng, Y. K., & Fang, M. H. (2017). MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2. International journal of hematology, 106(2), 258-265. https://doi.org/10.1007/s12185-017-2232-2
Ke, Shun, et al. "MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2." International journal of hematology vol. 106,2 (2017): 258-265. doi: https://doi.org/10.1007/s12185-017-2232-2
Ke S, Li RC, Lu J, Meng FK, Feng YK, Fang MH. MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2. Int J Hematol. 2017 Aug;106(2):258-265. doi: 10.1007/s12185-017-2232-2. Epub 2017 Apr 13. PMID: 28409330.
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Int J Hematol. 2017 Aug;106(2):258-265. doi: 10.1007/s12185-017-2232-2. Epub 2017 Apr 13.

MicroRNA-192 regulates cell proliferation and cell cycle transition in acute myeloid leukemia via interaction with CCNT2.

International journal of hematology

Shun Ke, Rui-Chao Li, Jun Lu, Fan-Kai Meng, Yi-Kuan Feng, Ming-Hao Fang

Affiliations

  1. Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  2. Department of General Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  3. Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
  4. Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. [email protected].

PMID: 28409330 DOI: 10.1007/s12185-017-2232-2

Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs approximately 18-22 nucleotides in length, which play an important role in malignant transformation. The roles of miR-192 as an oncogene or tumor suppressor in solid tumors have been previously reported. However, little is known about the role of miR-192 in human acute myeloid leukemia. The results of the present study indicate that miR-192 is significantly downregulated in specimens from acute myeloid leukemia patients. Functional assays demonstrated that overexpression of miR-192 in NB4 and HL-60 cells significantly inhibited cell proliferation compared with that in control cells, and induced G0/G1 cell cycle arrest, cell differentiation, and apoptosis in vitro. Dual-luciferase reporter gene assays showed that miR-192 significantly suppressed the activity of a reporter gene containing the wild type 3'-UTR of CCNT2, but it did not suppress the activity of a reporter gene containing mutated 3'-UTR of CCNT2. QRT-PCR and Western blot assays showed that miR-192 significantly downregulated the expression of CCNT2 in human leukemia cells. Exogenous expression of CCNT2 attenuated the cell cycle arrest induced by miR-192 in NB4 and HL-60 cells. Collectively, miR-192 inhibits cell proliferation and induces G0/G1 cell cycle arrest in AML by regulating the expression of CCNT2.

Keywords: Acute myeloid leukemia; CCNT2; Cell cycle; miR-192

References

  1. Oncol Rep. 2014 May;31(5):2035-42 - PubMed
  2. Tumour Biol. 2015 May;36(5):3791-7 - PubMed
  3. Oncogene. 2002 Jun 13;21(26):4158-65 - PubMed
  4. Lancet. 2006 Nov 25;368(9550):1894-907 - PubMed
  5. Cancer. 2008 Jan 1;112(1):4-16 - PubMed
  6. Blood. 2007 Jan 15;109(2):431-48 - PubMed
  7. Oncol Rep. 2014 Apr;31(4):1863-70 - PubMed
  8. Am J Pathol. 2014 Apr;184(4):996-1009 - PubMed
  9. J Cell Physiol. 2006 Apr;207(1):232-7 - PubMed
  10. EMBO J. 2008 Jul 9;27(13):1907-18 - PubMed
  11. Cell Cycle. 2016;15(2):196-212 - PubMed
  12. Oncol Rep. 2013 Jul;30(1):276-84 - PubMed
  13. Cell. 2013 Apr 25;153(3):516-9 - PubMed
  14. J Gene Med. 2016 Aug 24;:null - PubMed
  15. Cancer. 1982 Mar 1;49(5):916-20 - PubMed
  16. Int J Oncol. 2014 Jul;45(1):383-92 - PubMed
  17. J Exp Clin Cancer Res. 2015 Jul 01;34:68 - PubMed
  18. PLoS One. 2013 Nov 01;8(11):e78713 - PubMed
  19. Blood. 1998 Oct 1;92(7):2322-33 - PubMed
  20. Genes Dev. 1998 Mar 1;12(5):755-62 - PubMed
  21. Nucleic Acids Res. 2011 Aug;39(15):6669-78 - PubMed
  22. BMC Cancer. 2013 Jul 29;13:364 - PubMed
  23. Oncol Rep. 2015 May;33(5):2176-82 - PubMed
  24. N Engl J Med. 1999 Sep 30;341(14):1051-62 - PubMed
  25. Int J Clin Exp Pathol. 2015 Jul 01;8(7):8048-56 - PubMed
  26. Carcinogenesis. 2013 Apr;34(4):803-11 - PubMed
  27. Cancer Lett. 2013 Jul 1;334(2):211-20 - PubMed
  28. J Cancer Res Clin Oncol. 2016 Jan;142(1):77-87 - PubMed
  29. Oncogene. 2014 Nov 13;33(46):5332-40 - PubMed
  30. Nature. 2001 Nov 15;414(6861):322-5 - PubMed

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