Display options
Cite
Long LM, He BF, Huang GQ, et al. microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2. Oncol Lett. 2014;9(2):645-650doi: 10.3892/ol.2014.2746.
Long, L. M., He, B. F., Huang, G. Q., Guo, Y. H., Liu, Y. S., & Huo, J. R. (2015). microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2. Oncology letters, 9(2), 645-650. https://doi.org/10.3892/ol.2014.2746
Long, Li-Min, et al. "microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2." Oncology letters vol. 9,2 (2015): 645-650. doi: https://doi.org/10.3892/ol.2014.2746
Long LM, He BF, Huang GQ, Guo YH, Liu YS, Huo JR. microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2. Oncol Lett. 2015 Feb;9(2):645-650. doi: 10.3892/ol.2014.2746. Epub 2014 Nov 28. PMID: 25621032; PMCID: PMC4301474.
Copy Download .nbib Format: NLM
Share it on

Oncol Lett. 2015 Feb;9(2):645-650. doi: 10.3892/ol.2014.2746. Epub 2014 Nov 28.

microRNA-214 functions as a tumor suppressor in human colon cancer via the suppression of ADP-ribosylation factor-like protein 2.

Oncology letters

Li-Min Long, Ben-Fu He, Guo-Qing Huang, Yong-Hong Guo, You-Shuo Liu, Ji-Rong Huo

Affiliations

  1. Department of Geriatrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
  2. Department of Oncology, 421 Hospital of the People's Liberation Army, Guangzhou, Guangdong 510318, P.R. China.
  3. Department of Emergency, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
  4. Department of Gastroenterology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.

PMID: 25621032 PMCID: PMC4301474 DOI: 10.3892/ol.2014.2746

Abstract

microRNAs (miRNAs/miRs) are a conserved class of endogenous, short non-coding RNAs that post-transcriptionally regulate the expression of genes involved in diverse cellular processes. miR-214 has been reported to be associated with several cancers, including human colon cancer. However, the function of miR-214 in colon cancer development is poorly understood. In the current study, miR-214 was demonstrated to be downregulated in colon cancer tissues compared with healthy colon tissues. Functional studies showed that miR-214 overexpression results in the inhibition of cell viability, colony formation and proliferation, and the induction of cell apoptosis. ADP-ribosylation factor-like protein 2 (ARL2) is predicted to be a target candidate of miR-214. A luciferase reporter assay, western blot analysis and quantitative polymerase chain reaction were performed, which revealed that miR-214 negatively regulates ARL2 expression by targeting its 3' untranslated region directly. In conclusion, the results of the present study revealed that miR-214 suppresses colon cancer cell growth via the suppression of ARL2, and indicated that miR-214 may present a significant potential therapeutic target for colon cancer.

Keywords: ADP-ribosylation factor-like protein 2; apoptosis; human colon cancer; miR-214; proliferation

References

  1. Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9779-84 - PubMed
  2. PLoS One. 2012;7(2):e31518 - PubMed
  3. Exp Cell Res. 2007 Feb 1;313(3):473-85 - PubMed
  4. Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 - PubMed
  5. Cancer Lett. 2011 May 1;304(1):52-9 - PubMed
  6. J Biol Chem. 2011 Mar 18;286(11):9468-76 - PubMed
  7. PLoS One. 2010 Jan 21;5(1):e8836 - PubMed
  8. Nature. 2004 Sep 16;431(7006):350-5 - PubMed
  9. Nucleic Acids Res. 2012 Jan;40(2):761-74 - PubMed
  10. Biochem Soc Trans. 2005 Dec;33(Pt 6):1269-72 - PubMed
  11. Nucleic Acids Res. 2008 Jan;36(Database issue):D165-9 - PubMed
  12. EMBO J. 2011 May 18;30(10):1990-2007 - PubMed
  13. Hepatology. 2010 Nov;52(5):1731-40 - PubMed
  14. J Biol Chem. 2013 Feb 8;288(6):4035-47 - PubMed
  15. Cell. 2004 Jan 23;116(2):281-97 - PubMed
  16. Cell Cycle. 2008 Oct;7(19):3074-82 - PubMed
  17. Mol Cancer Res. 2011 Jul;9(7):824-33 - PubMed
  18. Biochem Biophys Res Commun. 2011 Aug 5;411(3):586-92 - PubMed
  19. Cancer Res. 2008 Jan 15;68(2):425-33 - PubMed
  20. J Hepatol. 2012 Sep;57(3):584-91 - PubMed
  21. EMBO J. 2011 May 18;30(10):1880-1 - PubMed
  22. Carcinogenesis. 2012 Jan;33(1):220-5 - PubMed
  23. J Biol Chem. 2012 Apr 20;287(17):14301-9 - PubMed
  24. RNA. 2003 Jan;9(1):112-23 - PubMed

Publication Types