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Bioinformatics analysis reveals potential candidate drugs for cervical cancer.

AbstractAIM:
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.
MATERIAL AND 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.
AuthorsZhihong Ai, Juan Wang, Yanli Xu, Yincheng Teng
JournalThe journal of obstetrics and gynaecology research (J Obstet Gynaecol Res) Vol. 39 Issue 5 Pg. 1052-8 (May 2013) ISSN: 1447-0756 [Electronic] Australia
PMID23551598 (Publication Type: Journal Article)
Copyright© 2013 The Authors. Journal of Obstetrics and Gynaecology Research © 2013 Japan Society of Obstetrics and Gynecology.
Chemical References
  • Antineoplastic Agents
  • Epidermal Growth Factor
Topics
  • Antineoplastic Agents (therapeutic use)
  • Carcinoma (drug therapy, metabolism)
  • Cell Proliferation
  • Computational Biology
  • Epidermal Growth Factor (antagonists & inhibitors, metabolism)
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic (drug effects)
  • Humans
  • MAP Kinase Signaling System (drug effects)
  • Molecular Targeted Therapy
  • Tumor Cells, Cultured
  • Uterine Cervical Neoplasms (drug therapy, metabolism)

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