Display options
Cite
Lai XB, Nie YQ, Huang HL, et al. NIMA-related kinase 2 regulates hepatocellular carcinoma cell growth and proliferation. Oncol Lett. 2017;13(3):1587-1594doi: 10.3892/ol.2017.5618.
Lai, X. B., Nie, Y. Q., Huang, H. L., Li, Y. F., Cao, C. Y., Yang, H., Shen, B., & Feng, Z. Q. (2017). NIMA-related kinase 2 regulates hepatocellular carcinoma cell growth and proliferation. Oncology letters, 13(3), 1587-1594. https://doi.org/10.3892/ol.2017.5618
Lai, Xiao-Bo, et al. "NIMA-related kinase 2 regulates hepatocellular carcinoma cell growth and proliferation." Oncology letters vol. 13,3 (2017): 1587-1594. doi: https://doi.org/10.3892/ol.2017.5618
Lai XB, Nie YQ, Huang HL, Li YF, Cao CY, Yang H, Shen B, Feng ZQ. NIMA-related kinase 2 regulates hepatocellular carcinoma cell growth and proliferation. Oncol Lett. 2017 Mar;13(3):1587-1594. doi: 10.3892/ol.2017.5618. Epub 2017 Jan 18. PMID: 28454295; PMCID: PMC5403431.
Copy Download .nbib Format: NLM
Share it on

Oncol Lett. 2017 Mar;13(3):1587-1594. doi: 10.3892/ol.2017.5618. Epub 2017 Jan 18.

NIMA-related kinase 2 regulates hepatocellular carcinoma cell growth and proliferation.

Oncology letters

Xiao-Bo Lai, Yu-Qiang Nie, Hong-Li Huang, Ying-Fei Li, Chuang-Yu Cao, Hui Yang, Bo Shen, Zhi-Qiang Feng

Affiliations

  1. Department of Gastroenterology and Hepatology, The First Municipal People's Hospital of Guangzhou, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
  2. Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, Guangzhou, Guangdong 510180, P.R. China.
  3. Department of Gastroenterology, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510282, P.R. China.

PMID: 28454295 PMCID: PMC5403431 DOI: 10.3892/ol.2017.5618

Abstract

NIMA-related kinase 2 (Nek2) is often upregulated in human cancer and is important in regulating the cell cycle and gene expression, and maintaining centrosomal structure and function. The present study aimed to investigate the expression pattern, clinical significance, and biological function of Nek2 in hepatocellular carcinoma (HCC). mRNA and protein levels of Nek2 were examined in HCC and corresponding normal liver tissues. The MTT and soft agar colony formation assays, and flow cytometry were employed to assess the roles of Nek2 in cell proliferation and growth. In addition, western blot analysis was performed to assess the expression of cell cycle- and proliferation-related proteins. The results revealed that Nek2 was upregulated in HCC tissues and cell lines. The clinical significance of Nek2 expression was also analyzed. Inhibiting Nek2 expression by siRNA suppressed cell proliferation, growth, and colony formation in hepatocellular carcinoma cell line HepG2 cells, induced cell cycle arrest in the G2/M phase by retarding the S-phase, and promoted apoptosis. Furthermore, Nek2 depletion downregulated β-catenin expression in HepG2 cells and diminished expression of Myc proto-oncogene protein (c-Myc), cyclins D1, B1, and E and cyclin-dependent kinase 1, whilst increasing protein levels of p27. This demonstrates that overexpression of Nek2 is associated with the malignant evolution of HCC. Targeting Nek2 may inhibit HCC cell growth and proliferation through the regulation of β-catenin by the Wnt/β-catenin pathway and therefore may be developed as a novel therapeutic strategy to treat HCC.

Keywords: Nek2; cancer proliferation; hepatocellular carcinoma; wnt/β-catenin

References

  1. Radiat Res. 2004 Aug;162(2):128-35 - PubMed
  2. Oncotarget. 2015 May 10;6(13):11421-33 - PubMed
  3. Eur J Cancer. 2009 Nov;45(16):2759-67 - PubMed
  4. Mol Biol Cell. 2003 Jul;14(7):2844-60 - PubMed
  5. Gene. 2004 Mar 17;328:135-42 - PubMed
  6. Cancer Sci. 2010 May;101(5):1163-9 - PubMed
  7. EMBO J. 2000 Apr 17;19(8):1816-26 - PubMed
  8. Nature. 2013 Sep 19;501(7467):328-37 - PubMed
  9. Biol Pharm Bull. 2015;38(7):986-91 - PubMed
  10. Biomed Res Int. 2014;2014:621082 - PubMed
  11. Head Neck. 2008 Jul;30(7):946-63 - PubMed
  12. PLoS One. 2012;7(4):e35510 - PubMed
  13. Cancer Lett. 2006 Jun 18;237(2):155-66 - PubMed
  14. Mol Cell Biol. 2005 Feb;25(4):1309-24 - PubMed
  15. Am J Hematol. 2009 Dec;84(12 ):803-8 - PubMed
  16. Bioessays. 2013 Sep;35(9):804-9 - PubMed
  17. CA Cancer J Clin. 2015 Mar;65(2):87-108 - PubMed
  18. Cell Growth Differ. 1994 Jun;5(6):625-35 - PubMed
  19. Mol Biol Cell. 2014 Apr;25(7):977-91 - PubMed
  20. Cancer Res. 2002 Jun 1;62(11):3322-6 - PubMed
  21. Front Biosci (Landmark Ed). 2014 Jan 01;19:352-65 - PubMed
  22. J Biol Chem. 1995 May 26;270(21):12899-905 - PubMed
  23. World J Hepatol. 2015 May 28;7(9):1157-67 - PubMed
  24. Cancer Sci. 2009 Jan;100(1):111-6 - PubMed
  25. Oncogenesis. 2013 Sep 09;2:e69 - PubMed
  26. Int J Oncol. 2002 Mar;20(3):441-51 - PubMed
  27. J Biol Chem. 2007 Sep 7;282(36):26431-40 - PubMed
  28. World J Hepatol. 2015 May 28;7(9):1168-83 - PubMed
  29. N Engl J Med. 2011 Sep 22;365(12):1118-27 - PubMed
  30. Clin J Gastroenterol. 2015 Feb;8(1):1-9 - PubMed
  31. Oncogene. 2002 Sep 9;21(40):6184-94 - PubMed
  32. Cancer Res. 2007 Oct 15;67(20):9637-42 - PubMed

Publication Types