title: Bioinformatics analysis reveals potential candidate drugs for cervical cancer.
abstract: OBJECTIVE
  We sought to explore the mechanisms of cervical carcinoma response to epidermal growth factor (EGF), and then identify biologically active small molecules capable of targeting the sub-pathways that were dysregulated in cervical cancer cells in the response to EGF.
  
  
  METHODS
  Differentially expressed genes and pathways were analyzed based on the transcription profile of GSE6783, and then the differentially expressed molecules were further analyzed by several bioinformatics methods.
  
  
  RESULTS
  Our results suggested that EGF could promote cervical cancer cell proliferation through triggering the dysregulation of certain sub-pathways in the mitogen-activated protein kinase signaling pathway, p53 signaling pathway and pathways in cancer. Furthermore, our bioinformatics analysis revealed a total of 49 small molecules which may play a role in perturbing the response to EGF of cervical cancer cells.
  
  
  CONCLUSIONS
  Candidate drugs identified by our approach may provide the groundwork for a combination therapy approach for cervical cancer; however, further studies are still needed to make sure that the use of parthenolide or other anti-cancer agents is effective without inhibiting important host defense mechanisms in cervical cancer.
authors.affiliation: Department of Obstetrics and Gynecology, Shanghai Sixth People's Hospital, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Zhihong
authors.initials: Z
authors.lastname: Ai
authors.forename: Juan
authors.initials: J
authors.lastname: Wang
authors.forename: Yanli
authors.initials: Y
authors.lastname: Xu
authors.forename: Yincheng
authors.initials: Y
authors.lastname: Teng
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002277:Carcinoma / Q000188:drug therapy* / Q000378:metabolism; D049109:Cell Proliferation; D019295:Computational Biology; D004815:Epidermal Growth Factor / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D058990:Molecular Targeted Therapy; D014407:Tumor Cells, Cultured; D002583:Uterine Cervical Neoplasms / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D004815:Epidermal Growth Factor