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5-Aza-2’-deoxycytidine and 4-phenylbutyric acid exert a cooperative effect on the expression of miR-196b in chronic myeloid leukemia cells
LIU Yue SHUAI Chun LI Jie-sheng YIN Hong SONG Yan-bin MA Wen-li*
Acta Anatomica Sinica ›› 2014, Vol. 45 ›› Issue (4) : 521-524.
5-Aza-2’-deoxycytidine and 4-phenylbutyric acid exert a cooperative effect on the expression of miR-196b in chronic myeloid leukemia cells
Objective To study if 5-Aza-2’-deoxycytidine along or together with 4-phenylbutyric acid could affect miR-196b expression levels in chronic myeloid leukemia cells.
Methods K562 cells were treated with DNA methylation inhibitor 5-Aza-2’-deoxycytidine, histone deacetylase inhibitors 4-phenylbutyric acid separately and the combined treatment with both of them, then expression levels of miR-196b were detected using Real-time PCR. Results The half inhibition concentration of 4-phenylbutyric acid was 1.58mmol/L. Comparing with the expression level of miR-196b in normal human bone marrow cells, the expression levels of miR-196b were significantly lower in Aza group, PBA group and negative control cells and nearly consistent among three groups, and as high as normal cells in combined treatment group. Conclusion The expression level of miR-196b in K562 cells could not return to normal treated with 5-Aza-2’-deoxycytidine or 4-phenylbutyric acid separately, while could restore normal when treated with both agents, indicating that miR-196b expression level in K562 cells is related with both DNA methylation and histone acetylation.
miR-196b / Methylation / Histone acetylation / K562cell / Real-time PCR / Human
［1］Li J, Ohliger J, Pei M. Significance of epigenetic landscape in cartilage regeneration from the cartilage development and pathology perspective［J］. Stem Cells Dev, 2014, Apr 1.［Epub ahead of print］
［2］Choi JD, Lee JS. Interplay between epigenetics and genetics in cancer［J］. Genomics Inform, 2013, 11(4):164-173.
［3］Saito Y, Saito H, Liang G, et al. Epigenetic alterations and microRNA misexpression in cancer and autoimmune diseases: a Critical Review［J］. Clin Rev Allergy Immunol, 2013, Dec 21. ［Epub ahead of print］.
［4］Vrtacnik P, Marc J, Ostanek B. Epigenetic mechanisms in bone［J］. Clin Chem Lab Med, 2013, Dec.［Epub ahead of print］
［5］Suzuki H, Maruyama R, Yamamoto E, et al. Epigenetic alteration and microRNA dysregulation in cancer［J］. Front Genet, 2013, 4:258.
［6］Li Z, Huang H, Chen P, et al. miR-196b directly targets both HOXA9/MEIS1 oncogenes and FAS tumour suppressor in MLL-rearranged leukaemia［J］. Nat Commun, 2012,3:688.
［7］Hulf T, Sibbritt T, Wiklund ED, et al. Discovery pipeline for epigenetically deregulated miRNAs in cancer: integration of primary miRNA transcription［J］. BMC Genomics, 2011, 12:54.
［8］Shen J, Wang S, Zhang YJ, et al. Genome-wide aberrant DNA methylation of microRNA host genes in hepatocellular carcinoma［J］. Epigenetics, 2012, 7(11):1230-1237.
［9］Abe W, Nasu K, Nakada C, et al. miR-196b targets c-myc and Bcl-2 expression, inhibits proliferation and induces apoptosis in endometriotic stromal cells［J］. Hum Reprod, 2013, 28(3):750-761.
［10］Machova Polakova K, Koblihova J, Stopka T. Role of epigenetics in chronic myeloid leukemia［J］. Curr Hematol Malig Rep, 2013, 8(1):28-36.
［11］Liu Y, Shuai Ch, Li JSh, et al. Application of CCK-8 in detecting the growth inhibiting effect of 5-Aza-2’-deoxycytidine on chronic myeloid leukemia cells［J］. Acta Anatomica Sinica, 2014, 45(4): 582-584. (in Chinese)
刘玥，帅春，李杰生，等. 活细胞计数试剂盒在检测5-氮杂-2’-脱氧胞苷对慢性粒细胞白血病细胞的增殖抑制作用中的应用［J］. 解剖学报，2014,45（4）：582-584.
［12］Hashimoto Y, Akiyama Y, Yuasa Y. Multiple-to-multiple relationships between microRNAs and target genes in gastric cancer［J］. PLoS One, 2013, 8(5):e62589.
［13］Nguyen Khac F, Waill MC, Romana SP, et al. Identical abnormality of the short arm of chromosome 18 in two Philadelphia-positive chronic myelocytic leukemia patients with erythroblastic transformation, resulting in duplication of BCR-ABL1 fusion［J］. Cancer Genet Cytogenet, 2002, 138(1):22-26.
［14］Vu LP, Luciani L, Nimer SD. Histone-modifying enzymes: their role in the pathogenesis of acute leukemia and their therapeutic potential［J］. Int J Hematol, 2013, 97(2):198-209.
［15］Ren LP, Song GY, Hu ZJ, et al. The chemical chaperon 4-phenylbutyric acid ameliorates hepatic steatosis through inhibition of de novo lipogenesis in high-fructose-fed rats［J］. Int J Mol Med, 2009, 32(5):1029-1036.
［16］Dang W, Steffen KK, Perry R, et al. Histone H4 lysine 16 acetylation regulates cellular lifespan［J］. Nature, 2009,459(7248):802-807.
［17］Ferres-Marco D, Gutierrez-Garcia I, Vallejo DM, et al. Epigenetic silencers and Notch collaborate to promote malignant tumours by Rb silencing［J］. Nature, 2006,439(7075):430-436.
［18］Eden S, Hashimshony T, Keshet I, et al. DNA methylation models histone acetylation［J］. Nature, 1998,394(6696):842.
［19］Bueno MJ, Perez de Castro I, Gomez de Cedron M, et al. Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression［J］. Cancer Cell, 2008,13(6):496-506.
［20］Metcalf AM, Spurdle AB. Endometrial tumour BRAF mutations and MLH1 promoter methylation as predictors of germline mismatch repair gene mutation status: a literature review［J］. Fam Cancer, 2014, 13(1): 1-2.
［21］Zhang X, Li HM, Liu Z, et al. Loss of heterozygosity and methylation of multiple tumor suppressor genes on chromosome 3 in hepatocellular carcinoma［J］. J Gastroenterol, 2013, 48(1):132-143.
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