Int J Cancer 2008, 123: 2791–2797.CrossRefPubMed 36. Tran N, McLean T, Zhang XY, Zhao CJ, Thomson JM, O’Brien C, Rose B: MicroRNA expression profiles in head and neck cancer cell lines. Biochem Biophys Res Comm 2007, 358: 12–17.CrossRefPubMed 37. Yang N, Coukos G, Zhang L: MicroRNA epigenetic alterations in human cancer: One step forward in diagnosis and treatment. Int J Cancer 2008, 122:

963–968.CrossRefPubMed 38. Chan JA, Krichevsky AM, Kosik KS: MicroRNA-21 is an antiapoptotic factor in human glioblastoma cells. Cancer Res 2005, 65: 6029–6033.CrossRefPubMed 39. Weiler J, Hunziker J, Hall J: Anti-miRNA oligonucleotides (AMOs): ammunition to target miRNAs implicated in human disease? Gene Ther 2006, 13: 496–502.CrossRefPubMed 40. Takamizawa J, Konishi H, Yanagisawa K, Tomida S, Osada H, Endoh H, Harano T, Yatabe Y, Nagino M, Nimura Y, Mitsudomi PLX4032 T, Takahashi T: Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival. Cancer Res 2004, 64: 3753–3756.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions In our study, all authors have contributed significantly, and that all

authors are in agreement Selleckchem PXD101 with the content of the manuscript. Each author’s contribution to the paper:TY: First author, background literature search, data analysis, development of final manuscript XYW: Corresponding author, research Tideglusib instruction, data analysis, development of final manuscript. RGG: background

literature search, data analysis. AL: research instruction, development of final manuscript. SY: research instruction, background literature search. YTC: data analysis, background literature search. YMW: research instruction, development of final manuscript. CMW: research instruction, data analysis. XZY: background literature search, data analysis.”
“Introduction Multi-drug resistance (MDR) of tumor cells, including leukemia cells, is a defense mechanism for retaining homeostasis when they are damaged by cytotoxic drugs [1]. Tumor cells emerge a series of biological changes during the development of MDR in them. In molecular mechanism, occurrence of tumor cells’ MDR is because of expression of genes related drug resistance [2]. To investigate which genes were in regulation in MDR of tumor cells, we established the multi-drug resistance cells HL-60/MDR using acute myelocytic leukemia cell line HL-60 at previous study. Then we screened and cloned the MDR related genes in HL-60/MDR cells using differential hybridization and gene chip [3, 4] and found a novel gene HA117 (GeneBank: AY230154) which may be related to MDR[5]. In this study, adenovirus vectors were constructed with the HA117 gene (Adeasy-HA117) to investigate whether HA117 gene could increase the drug resistance in chronic myelogenous myeloid leukemia cell line K562.