Syndecan binding protein (SDCBP) is overexpressed in estrogen receptor negative breast cancers, and is a potential promoter for tumor proliferation

Syndecan binding protein (SDCBP), an adapter protein containing PDZ domains, contributes to the tumorigenicity and metastasis of many malignant tumors, such as malignant melanoma. Our study aimed in revealing the expression profile of SDCBP in breast cancer (BCa) and its role in tumor cell prolifera...

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Bibliographic Details
Published in:PloS one 2013-03, Vol.8 (3), p.e60046-e60046
Main Authors: Qian, Xiao-Long, Li, Ya-Qing, Yu, Bin, Gu, Feng, Liu, Fang-Fang, Li, Wei-Dong, Zhang, Xin-Min, Fu, Li
Format: Article
Language:English
Subjects:
17β-Estradiol
Adapters
Animals
Apoptosis
Biology
Biotechnology
Breast
Breast cancer
Breast Neoplasms - metabolism
Cancer metastasis
Cancer therapies
Cancer treatment
Care and treatment
Cell adhesion & migration
Cell culture
Cell cycle
Cell Line, Tumor
Cell proliferation
Chinese medicine
Cyclin E
Disease prevention
Down-regulation
Education
Epidermal growth factor
Epigenetics
Estradiol
Estrogen
Estrogen Receptor alpha - metabolism
Estrogen receptors
Estrogens
Female
Gene Expression Regulation, Neoplastic - genetics
Gene Expression Regulation, Neoplastic - physiology
Hospitals
Humans
Immunohistochemistry
In vivo methods and tests
Kinases
Laboratories
Medicine
Melanoma
Metastases
Metastasis
Mice
Mice, Inbred BALB C
Mice, Nude
Pathology
Phenols (Class of compounds)
Prostate
Protein binding
Proteins
Reverse Transcriptase Polymerase Chain Reaction
Sex hormones
Signal transduction
Signaling
Silence
Syndecan
Syntenins - genetics
Syntenins - metabolism
Tissues
Tumor cells
Tumorigenicity
Tumors
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Summary:Syndecan binding protein (SDCBP), an adapter protein containing PDZ domains, contributes to the tumorigenicity and metastasis of many malignant tumors, such as malignant melanoma. Our study aimed in revealing the expression profile of SDCBP in breast cancer (BCa) and its role in tumor cell proliferation, and then exploring its value in the targeted treatment of BCa. We first evaluated the SDCBP expression by immunohistochemistry in normal breast and BCa tissues. Then we explored the expression profile of SDCBP in different BCa cell lines. By constructing SDCBP-silenced BCa cell clones, we further assessed the effects of SDCBP suppression on tumor cells in vitro by cell culture and in vivo by tumorigenicity. SDCBP expression was detected in 80.6% (n = 160) of BCa tissues, in contrast to its expression in 13% (n = 23) of normal breast tissues (P
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0060046