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2014 | 19 | 1 |

Tytuł artykułu

MiR - 34a regulates apoptosis in liver cells by targeting the KLF4 gene

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
MicroRNAs (miRNAs) regulate gene expression by inhibiting translation or targeting messenger RNA (mRNA) for degradation in a posttranscriptional fashion. In this study, we show that ectopic expression of miR-34a-5p reduces the mRNA and protein levels of Krüppel-like factor 4 (KLF4). We also demonstrate that miR-34a targets the 3′-untranslated mRNA region of KLF4 and show that overexpression of miR-34a induces a significant level of apoptosis in BNL CL.2 cells exposed to doxorubicin or 10 Gy X-ray. Our data suggest that the effects of miR-34a on apoptosis occur due to the downregulation of KLF4.

Słowa kluczowe

Wydawca

-

Rocznik

Tom

19

Numer

1

Opis fizyczny

p.52-64,fig.,ref.

Twórcy

autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Cardiology, the First Affiliated Hospital of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Radiation Medicine, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou City, China
autor
  • Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai City, China

Bibliografia

  • 1. Bartel, D.P. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell 116 (2004) 281-297.
  • 2. Kim, V.N. MicroRNA biogenesis: coordinated cropping and dicing. Nat. Rev. Mol. Cell. Biol. 6 (2005) 376-385.
  • 3. Nilsen, T.W. Mechanisms of microRNA-mediated gene regulation in animal cells. Trends Genet. 23 (2007) 243-249.
  • 4. Sunkar, R., Chinnusamy, V., Zhu, J. and Zhu, J.K. Small RNAs as big players in plant abotic stress responses and nutrient deprivation. Trends Plant Sci. 12 (2007) 301-309.
  • 5. Kulshreshtha, R., Ferracin, M., Wojcik, S.E., Garzon, R., Alder, H., AgostoPerez, F.J., Davuluri, R., Liu, C.G., Croce, C.M., Negrini, M., Calin, G.A. and Ivan, M.A. microRNA signature of hypoxia. Mol. Cell. Biol. 27 (2007) 1859-1867.
  • 6. Trindade, I., Capitão, C., Dalmay, T., Fevereiro, M.P. and Santos, D.M. miR398 and miR408 are up-regulated in response to water deficit in Medicago truncatula. Planta 231 (2010) 705-716.
  • 7. Simone, N.L., Soule, B.P., Ly, D., Saleh, A.D., Savage, J.E., Degraff, W., Cook, J., Harris, C.C., Gius, D. and Mitchell, J.B. Ionizing radiation-induced oxidative stress alters miRNA expression. PLoS One 4 (2009) e6377.
  • 8. Chaudhry, M.A. Real-time PCR analysis of micro-RNA expression in ionizing radiation-treated cells. Cancer Biother. Radiopharm. 24 (2009) 49-56.
  • 9. Chaudhry, M.A. Biomarkers for human radiation exposure. J. Biomed. Sci. 15 (2008) 557-563.
  • 10. Leung, A.K.L. and Sharp, P.A. MicroRNA functions in stress responses. Mol. Cell 40 (2010) 205-215.
  • 11. Babar, I.A., Slack, F.J. and Weidhaas, J.B. MiRNA modulation of the cellular stress response. Future Oncol. 4 (2008) 289-298.
  • 12. Ichimura, A., Ruike, Y., Terasawa, K., Shimizu, K. and Tsujimoto, G. MicroRNA-34a inhibits cell proliferation by repressing mitogen-activated protein kinase 1 during megakaryocytic differentiation of K562 cells. Mol. Pharmacol. 77 (2010) 1016-1024.
  • 13. Sun, F., Fu, H., Liu, Q., Tie, Y., Zhu, J., Xing, R., Sun, Z. and Zheng, X. Downregulation of CCND1 and CDK6 by miR-34a induces cell cycle arrest. FEBS Lett. 582 (2008) 1564-1568.
  • 14. Jain, A.K., Allton, K., Iacovino, M., Mahen, E., Milczarek, R.J., Zwaka, T.P., Kyba, M. and Barton, M.C. p53 Regulates Cell Cycle and MicroRNAs to Promote Differentiation of Human Embryonic Stem Cells. PLoS Biol. 10 (2012) e1001268.
  • 15. Ji, X., Wang, Z., Geamanu, A., Goja, A., Sarkar, F.H. and Gupta, S.V. Delta-tocotrienol suppresses Notch-1 pathway by up-regulating miR-34a in non-small cell lung cancer cells. Int. J. Cancer 131 (2012) 2668-2677.
  • 16. Chang, T.C., Wentzel, E.A., Kent, O.A., Ramachandran, K., Mullendore, M., Lee, K.H., Feldmann, G., Yamakuchi, M., Ferlito, M., Lowenstein, C.J., Arking, D.E., Beer, M.A., Maitra, A. and Mendell, J.T. Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Mol. Cell 26 (2007) 745-752.
  • 17. Hermeking, H. The miR-34 family in cancer and apoptosis. Cell Death Differ. 17 (2010) 193-199.
  • 18. Krek, A., Grün, D., Poy, M.N., Wolf, R., Rosenberg, L., Epstein, E.J., MacMenamin, P., da Piedade, I., Gunsalus, K.C., Stoffel, M. and Rajewsky, N. Combinatorial microRNA target predictions. Nat. Genet. 37 (2005) 495-500.
  • 19. Ghaleb, A.M., Katz, J.P., Kaestner, K.H., Du, J.X. and Yang, V.W. Krüppellike factor 4 exhibits antiapoptotic activity following gamma-radiationinduced DNA damage. Oncogene 26 (2007) 2365-2373.
  • 20. http://www.genepharma.com/En/productslist.asp?Parentid=15&sortname=m iRNA
  • 21. http://www.microrna.org/microrna/home.do
  • 22. http://www.mirbase.org
  • 23. http://pictar.mdc-berlin.de
  • 24. Xia, J., Duan, Q., Ahmad, A., Bao, B., Benerjee, S., Shi, Y., Ma, J., Geng, J., Chen, Z., Rahman, K.M., Miele, L., Sarkar, F.H. and Wang, Z. Genistein inhibits cell growth and induces apoptosis through up-regulation of miR-34a in pancreatic cancer cells. Curr. Drug Targets 13 (2012) 1750-1756.
  • 25. Sacher, G.A. Dependence of acute radiosensitivity on age in adult female mouse. Science 125 (1957) 1039-1040.
  • 26. Crosfill, M.L., Lindop, P.J. and Rotblat, J. Variation of sensitivity to ionizing radiation with age. Nature 183 (1959) 1729-1730.
  • 27. Burdelya, L.G., Krivokrysenko, V.I., Tallant, T.C., Strom, E., Gleiberman, A.S., Gupta, D., Kurnasov, O.V., Fort, F.L., Osterman, A.L., Didonato, J.A., Feinstein, E. and Gudkov, A.V.. An agonist of toll-like receptor 5 has radioprotective activity in mouse and primate models. Science 320 (2008) 226-230.
  • 28. Lewanski, C.R. and Gullick, W.J. Radiotherapy and cellular signaling. Lancet Oncol. 2 (2001) 366-370.
  • 29. Peter, M.E. Targeting of mRNAs by multiple miRNAs: the next step. Oncogene 29 (2010) 2161-2164.
  • 30. Kloosterman, W.P. and Plasterk, R.H. The diverse functions of microRNAs in animal development and disease. Dev. Cell 11 (2006) 441-450.
  • 31. Esquela-Kerscher, A. and Slack, F.J. Oncomirs-microRNAs with a role in cancer. Nat. Rev. Cancer 6 (2006) 259-269.
  • 32. Thalia, A.F, Jessica, I.H., Pavel, M. and Thomas, T. microRNAs in Human Cancer . Adv. Exp. Med. Biol. 774 (2013) 1-20.
  • 33. Metheetrairut, C. and Slack, F.J. MicroRNAs in the ionizing radiation response and in radiotherapy. Curr. Opin. Genet. Dev. 23 (2013) 12-19.
  • 34. Chang, T.C., Wentzel, E.A., Kent, O.A., Ramachandran, K., Mullendore, M., Lee, K.H, Feldmann, G., Yamakuchi, M., Ferlito, M., Lowenstein, C.J., Arking, D.E., Beer, M.A., Maitra, A. and Mendell, J.T. Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Mol. Cell 26 (2007) 745-752.
  • 35. Raver-Shapira, N., Marciano, E., Meiri, E., Spector, Y., Rosenfeld, N., Moskovits, N., Bentwich, Z. and Oren, M. Transcriptional activation of miR-34a contributes to p53-mediated apoptosis. Mol. Cell 26 (2007) 731-743.
  • 36. Zhang, W., Shields, J.M., Sogawa, K., Fujii-Kuriyama, Y. and Yang, V.W. The gut-enriched Kruppel-like factor suppresses the activity of the CYP1A1 promoter in a Spl-dependent fashion. J. Biol. Chem. 273 (1998) 17917-17925.
  • 37. Yoon, H.S., Chen, X. and Yang, V.W. Kruppel-like factor 4 mediates p53- dependent G1/S cell cycle arrest in response to DNA damage. J. Biol. Chem. 278 (2003) 2101-2105.
  • 38. Yoon, H.S. and Yang, V.W. Requirement of Kruppel-like factor 4 in preventing entry into mitosis following DNA damage. J. Biol. Chem. 279 (2004) 5035-5041.
  • 39. Calin, G.A. and Croce, C.M. MicroRNA-cancer connection: the beginning of a new tale. Cancer Res. 66 (2006) 7390-7394.
  • 40. Hammond, S.M. MicroRNAs as oncogenes. Curr. Opin. Genet. Dev. 16 (2006) 4-9.
  • 41. Bommer, G.T., Gerin, I., Feng, Y., Kaczorowski, A.J., Kuick, R., Love, R.E., Zhai, Y., Giordano, T.J., Qin, Z.S., Moore, B.B., MacDougald, O.A., Cho, K.R. and Fearon, E.R. P53-mediated activation of miRNA34 candidate tumor-suppressor genes. Curr. Biol. 17 (2007) 1298-1307.
  • 42. Fan, F., Sun, A., Zhao, H., Liu, X., Zhang, W., Jin, X., Wang, C., Ma, X., Shen, C., Zou, Y., Hu, K. and Ge, J. MicroRNA-34a promotes cardiomyocyte apoptosis post myocardial infarction through down-regulating aldehyde dehydrogenase 2. Curr. Pharm. Des. 19 (2013) 4865-4873.
  • 43. Sasaki, A., Udaka, Y., Tsunoda, Y., Yamamoto, G., Tsuji, M., Oyamada, H., Oguchi, K. and Mizutani, T. Analysis of p53 and miRNA expression after irradiation of glioblastoma cell lines. Anticancer Res. 32 (2012) 4709-4713.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

bwmeta1.element.agro-5b4cd85a-5f2a-48f4-8cad-fa198cd853fd
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