title: Gene network exploration of crosstalk between apoptosis and autophagy in chronic myelogenous leukemia.
abstract: BACKGROUND
  Gene expression levels change to adapt the stress, such as starvation, toxin, and radiation. The changes are signals transmitted through molecular interactions, eventually leading to two cellular fates, apoptosis and autophagy. Due to genetic variations, the signals may not be effectively transmitted to modulate apoptotic and autophagic responses. Such aberrant modulation may lead to carcinogenesis and drug resistance. The balance between apoptosis and autophagy becomes very crucial in coping with the stress. Though there have been evidences illustrating the apoptosis-autophagy interplay, the underlying mechanism and the participation of the regulators including transcription factors (TFs) and microRNAs (miRNAs) remain unclear.
  
  
  RESULTS
  Gene network is a graphical illustration for exploring the functional linkages and the potential coordinate regulations of genes. Microarray dataset for the study of chronic myeloid leukemia was obtained from Gene Expression Omnibus. The expression profiles of those genes related to apoptosis and autophagy, including MCL1, BCL2, ATG, beclin-1, BAX, BAK, E2F, cMYC, PI3K, AKT, BAD, and LC3, were extracted from the dataset to construct the gene networks.
  
  
  CONCLUSIONS
  The network analysis of these genes explored the underlying mechanisms and the roles of TFs and miRNAs for the crosstalk between apoptosis and autophagy.
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: Fengfeng
authors.identifier: 0000-0003-4959-4527
authors.initials: F
authors.lastname: Wang
authors.affiliation: Department of Clinical Oncology, Queen Elizabeth Hospital, 30 Gascoigne Road, Kowloon, Hong Kong.
authors.forename: William C S
authors.initials: WC
authors.lastname: Cho
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: Lawrence W C
authors.initials: LW
authors.lastname: Chan
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: S C Cesar
authors.initials: SC
authors.lastname: Wong
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: Nancy B Y
authors.initials: NB
authors.lastname: Tsui
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: Parco M
authors.initials: PM
authors.lastname: Siu
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: S P
authors.initials: SP
authors.lastname: Yip
authors.affiliation: Department of Health Technology and Informatics, Hong Kong Polytechnic University, Lee Shau Kee Building, Hung Hom, Kowloon, Hong Kong.
authors.forename: Benjamin Y M
authors.initials: BY
authors.lastname: Yung
mesh_terms: D017209:Apoptosis; D001343:Autophagy; D003198:Computer Simulation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000378:metabolism* / Q000473:pathology; D008954:Models, Biological; D009363:Neoplasm Proteins / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D009363:Neoplasm Proteins
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