PMID- 25832863
OWN - NLM
STAT- MEDLINE
DCOM- 20160302
LR  - 20181113
IS  - 1559-131X (Electronic)
IS  - 1357-0560 (Linking)
VI  - 32
IP  - 5
DP  - 2015 May
TI  - Identification of potential therapeutic target genes, key miRNAs and mechanisms 
      in acute myeloid leukemia based on bioinformatics analysis.
PG  - 152
LID - 10.1007/s12032-015-0572-4 [doi]
AB  - The study was aimed to explore the underlying mechanisms and identify the 
      potential target genes and key miRNAs for acute myeloid leukemia (AML) treatment 
      by bioinformatics analysis. The microarray data of GSE9476 were downloaded from 
      Gene Expression Omnibus database. A total of 64 samples, including 26 AML and 38 
      normal samples, were used to identify differentially expressed genes (DEGs) 
      between AML and normal samples. The functional enrichment analysis was performed, 
      and protein-protein interaction (PPI) network of the DEGs was constructed by 
      Cytoscape software. Besides, the target miRNAs for DEGs were identified. Totally, 
      323 DEGs were identified, including 87 up-regulated and 236 down-regulated genes. 
      Not only up-regulated genes but also down-regulated genes were related to 
      hematopoietic-related functions. Besides, down-regulated genes were also enriched 
      in primary immunodeficiency pathway. Tumor necrosis factor (TNF), interleukin 7 
      receptor (IL7R), lymphocyte-specific protein tyrosine kinase (LCK), CD79a 
      molecule and immunoglobulin-associated alpha (CD79A) were identified in these 
      functions. TNF and LCK were hub nodes in PPI networks. miR-124 and miR-181 were 
      important miRNAs in this study. The hematopoietic-related functions and primary 
      immunodeficiency pathway may be associated with AML development. Genes, such as 
      TNF, IL7R, LCK and CD79A, may be potential therapeutic target genes for AML, and 
      miR-124 and miR-181 may be key miRNAs in AML development.
FAU - Zhao, Yanhong
AU  - Zhao Y
AD  - Department of Hematology, The First Affiliated Hospital of Harbin Medical 
      University, No. 23, Youzheng Street, Nangang District, Harbin, 150001, China, 
      hanyunf2@163.com.
FAU - Zhang, Xuefang
AU  - Zhang X
FAU - Zhao, Yanqiu
AU  - Zhao Y
FAU - Kong, Desheng
AU  - Kong D
FAU - Qin, Fan
AU  - Qin F
FAU - Sun, Jing
AU  - Sun J
FAU - Dong, Ying
AU  - Dong Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150402
PL  - United States
TA  - Med Oncol
JT  - Medical oncology (Northwood, London, England)
JID - 9435512
RN  - 0 (CD79 Antigens)
RN  - 0 (MIRN124 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Receptors, Interleukin-7)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.10.2 (Lymphocyte Specific Protein Tyrosine Kinase p56(lck))
SB  - IM
MH  - CD79 Antigens/genetics
MH  - Computational Biology/methods
MH  - Databases, Genetic
MH  - Down-Regulation/genetics
MH  - Gene Expression/genetics
MH  - Gene Expression Profiling/methods
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - Humans
MH  - Leukemia, Myeloid, Acute/*genetics
MH  - Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics
MH  - MicroRNAs/*genetics
MH  - Protein Interaction Domains and Motifs/genetics
MH  - Receptors, Interleukin-7/genetics
MH  - Software
MH  - Tumor Necrosis Factor-alpha/genetics
MH  - Up-Regulation/genetics
EDAT- 2015/04/04 06:00
MHDA- 2016/03/05 06:00
CRDT- 2015/04/03 06:00
PHST- 2015/03/11 00:00 [received]
PHST- 2015/03/13 00:00 [accepted]
PHST- 2015/04/03 06:00 [entrez]
PHST- 2015/04/04 06:00 [pubmed]
PHST- 2016/03/05 06:00 [medline]
AID - 10.1007/s12032-015-0572-4 [doi]
PST - ppublish
SO  - Med Oncol. 2015 May;32(5):152. doi: 10.1007/s12032-015-0572-4. Epub 2015 Apr 2.