Document Detail

Luteinizing hormone facilitates angiogenesis in ovarian epithelial tumor cells and metformin inhibits the effect through the mTOR signaling pathway.
MedLine Citation:
PMID:  22469973     Owner:  NLM     Status:  Publisher    
High levels of gonadotropin are a risk factor for ovarian cancer development. Aberrant gonadotropin levels benefit tumor angiogenesis, but the detailed mechanism is not clear. Therefore, the aim of this study was to investigate the molecular mechanism of high levels of luteinizing hormone (LH) on the promotion of tumor angiogenesis and to outline a feasible therapeutic strategy. Western blotting and immunofluorescence staining were used to determine the effect of LH on VEGF and slit2 expression and examine the signaling pathway involved in regulating the expression of both molecules. Real-time PCR was used to investigate the effect of metformin on LH induction of VEGF and slit2 expression. It was found that 50 mIU/ml LH significantly upregulated VEGF and slit2 expression, and activated the PI3K/AKT-mTOR signaling pathway. However, metformin inhibited the mTOR signaling pathway and further blocked LH-induced VEGF and slit2 expression. In conclusion, high levels of LH promote angiogenesis in ovarian cancer via the PI3K/AKT-mTOR pathway. However, metformin could inhibit tumor angiogenesis by blocking the mTOR signaling pathway.
Hong Liao; Qian Zhou; Yanqiong Gu; Tao Duan; Youji Feng
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-3-27
Journal Detail:
Title:  Oncology reports     Volume:  -     ISSN:  1791-2431     ISO Abbreviation:  -     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-4-3     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9422756     Medline TA:  Oncol Rep     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, P.R. China.
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