| S-phase reduction in T47D human breast cancer epithelial cells induced by an S100P antisense-retroviral construct. | |
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MedLine Citation:
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PMID: 17273741 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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S100P is expressed in several malignant neoplasms. It was previously demonstrated that S100P is involved in the very early stages of breast carcinogenesis. In the present study we used a retrovirus-mediated transfer of antisense-S100P in order to check whether the decrease in expression of this protein could lead to alterations in the cell cycle of epithelial cells of human breast cancer. The T47D breast carcinoma cell line, a human breast epithelial cell that expresses high levels of S100P, was a tool used in this study to investigate the alteration in cell cycle induced by a retrovirus-mediated transfer of antisense-S100P. First we used the real-time PCR technique to quantify the gene expression. The results showed a reduction of 63% of expression within the T47D-S100P-A/S infected population compared with control T47D-LXSN clones. To determine the impact of the S100P antisense technique on protein expression in T47D cells, we performed immunofluorescence staining and analyzed the resulting images using a confocal microscope. The images showed much less pronounced antibody marking of the S100P protein in the T47D-S100P-A/S compared with control cells. To evaluate whether the antisense approach caused any alteration in the cell cycle, we concluded the study with flow cytometric analysis of the cell distribution. Our findings indicated that, in our model, S100P-antisense cells showed a 23% reduction of cells at the S-phase. Using transduction techniques with an S100P antisense-retroviral construct we were able to demonstrate a significant reduction in S-phase of the T47D cell cycle. To the best of our knowledge, this is the first time that an antisense approach has been used against S100P mRNA in breast cancer epithelial cells. The results showed here seem to further classify S100P as a protein that might be involved in the cell cycle imbalance observed during breast carcinogenesis. |
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Authors:
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Bettina Beissel; Ismael D C G Silva; João B Pesquero; Jose Russo; Nestor Schor; Maria Helena Bellini |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Oncology reports Volume: 17 ISSN: 1021-335X ISO Abbreviation: Oncol. Rep. Publication Date: 2007 Mar |
Date Detail:
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Created Date: 2007-02-02 Completed Date: 2007-05-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9422756 Medline TA: Oncol Rep Country: Greece |
Other Details:
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Languages: eng Pagination: 611-5 Citation Subset: IM |
Affiliation:
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Centro de Química e Meio Ambiente, IPEN/CNEN-SP, 04039-032 São Paulo, SP, Brazil. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Breast Neoplasms
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metabolism* Calcium-Binding Proteins / antagonists & inhibitors*, genetics, metabolism Cell Cycle / physiology* Cell Line, Tumor Epithelial Cells / metabolism* Female Flow Cytometry Fluorescent Antibody Technique Gene Expression Humans Microscopy, Confocal Neoplasm Proteins / antagonists & inhibitors*, genetics, metabolism RNA, Antisense* Retroviridae / genetics Reverse Transcriptase Polymerase Chain Reaction |
| Chemical | |
Reg. No./Substance:
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0/Calcium-Binding Proteins; 0/Neoplasm Proteins; 0/RNA, Antisense; 0/S100P protein, human |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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