Abstract | AIM: 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.
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Authors | Zhihong Ai, Juan Wang, Yanli Xu, Yincheng Teng |
Journal | The journal of obstetrics and gynaecology research
(J Obstet Gynaecol Res)
Vol. 39
Issue 5
Pg. 1052-8
(May 2013)
ISSN: 1447-0756 [Electronic] Australia |
PMID | 23551598
(Publication Type: Journal Article)
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Copyright | © 2013 The Authors. Journal of Obstetrics and Gynaecology Research © 2013 Japan Society of Obstetrics and Gynecology. |
Chemical References |
- Antineoplastic Agents
- Epidermal Growth Factor
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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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