Document Detail

Bone morphogenetic protein 6 inhibit stress-induced breast cancer cells apoptosis via both Smad and p38 pathways.
MedLine Citation:
PMID:  17879955     Owner:  NLM     Status:  MEDLINE    
Breast carcinoma is one of the most common malignant tumors and has become a more common cancer in women. BMP6 was abnormally expressed in breast cancer specimens and cell lines. However, the contribution of BMP6 in promoting breast cancer progression remains unknown. The purpose of our study was to establish whether expression of BMP6 in breast cancer cells affect their proliferation or apoptosis and the mechanism. We found that BMP6 inhibited proliferation of MDA-MB-231 cells and blocked cell cycle at G(0)/G(1) stage. BMP6 also inhibited serum deprivation induced apoptosis in MDA-MB-231 cells. At the 4 days of serum starvation, BMP6 reduced the percentage of caspase-3 positive cells from 49% to 21%, BMP6 also reduced sub-G(1) peak induced by serum starvation. In contrast, BMP6 significantly enhanced survivin expression both at mRNA and protein levels. Dominant negative-survivin and Antisense-survivin impaired BMP6 induced antiapoptotic effect. BMP6 enhanced survivin expression at the transcription level in a Smad-dependent manner. BMP6 also played its antiapoptotic effect through activation p38 MAPK signal pathway, independent of smad/survivin pathway. These results suggested that BMP6 induced cell cycle arrest in estrogen-insensitive breast cancer cells. BMP6 inhibits stress-induced apoptosis via both Smad and p38 signal pathways.
Jun Du; Shuang Yang; Zhaoqi Wang; Chunli Zhai; Wei Yuan; Rongyue Lei; Jie Zhang; Tianhui Zhu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular biochemistry     Volume:  103     ISSN:  1097-4644     ISO Abbreviation:  J. Cell. Biochem.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-04-02     Completed Date:  2008-07-16     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8205768     Medline TA:  J Cell Biochem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1584-97     Citation Subset:  IM    
Copyright Information:
2007 Wiley-Liss, Inc.
Medical College of Nankai University, Tianjin, China.
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MeSH Terms
Apoptosis* / drug effects
Bone Morphogenetic Protein 6
Bone Morphogenetic Proteins / metabolism*,  pharmacology
Breast Neoplasms / metabolism*
Caspase 3 / metabolism
Cell Line, Tumor
G0 Phase / drug effects
G1 Phase / drug effects
Gene Expression Regulation, Neoplastic / drug effects
MAP Kinase Signaling System* / drug effects
Microtubule-Associated Proteins / biosynthesis
Neoplasm Proteins / biosynthesis
RNA, Messenger / biosynthesis
Smad Proteins / metabolism*
Time Factors
p38 Mitogen-Activated Protein Kinases / metabolism*
Reg. No./Substance:
0/BIRC5 protein, human; 0/BMP6 protein, human; 0/Bone Morphogenetic Protein 6; 0/Bone Morphogenetic Proteins; 0/Microtubule-Associated Proteins; 0/Neoplasm Proteins; 0/RNA, Messenger; 0/Smad Proteins; EC Mitogen-Activated Protein Kinases; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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