| Histological type of oncogenity and expression of cell cycle genes in tumor cells from human mesenchymal stem cells. | |
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MedLine Citation:
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PMID: 17016587 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In previous experiments, a novel tumor cell line, which was characterized by dominated F6 mutated from human mesenchymal stem cells (hMSCs), was developed. The mechanism and biological characteristics of this mutation are still unclear. In this study, the histological type of F6 cells was investigated by immunohistochemistry with specific markers: vimentin, CD117, desmin, NSE and vWF. The characteristics of proliferation and metastasis were shown by PCNA (proliferating cell nuclear antigen), and nm23 and cell cycle-related genes, such as p16, p21, p53 and pRb, were analyzed by RT-PCR and immunohistochemistry. The expression of hTRAP and BMI-1 were detected by real-time PCR and Western blotting. The activity of telomerase was analyzed by TRAP (telomerase repeat amplification protocol) assay. The results showed that multi-directional differentiation occurred in F6 cells, i.e., special markers of muscle, endothelial cell and nerve system were co-expressed in F6 cells, while hardly expressed in hMSCs. F6 cells maintained the same properties as of MSCs, such as negativity for both CD117 and vimentin. F6 cells exhibited strong positivity for PCNA and negativity for nm23. The cell cycle-related genes, such as p16, p21, p53 and pRb, were not detected in F6 cells, while the expression of hTRAP and BMI-1 was significantly higher. The activity of telomerase was also significantly higher in F6 cells than that in hMSCs. These findings indicated that multi-directional differentiation occurred during the transformation of hMSCs into F6 cells, and that the genes of cell cycle and cell senescence may also be associated with the neoplasia of adult stem cells. |
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Authors:
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Runqiu Jiang; Wenrong Xu; Wei Zhu; Miao Chen; Hui Qian; Chun Qiao; Huan Yang; Xingzhong Wang; Yongchang Chen |
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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: 16 ISSN: 1021-335X ISO Abbreviation: Oncol. Rep. Publication Date: 2006 Nov |
Date Detail:
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Created Date: 2006-10-03 Completed Date: 2007-01-09 Revised Date: 2009-11-19 |
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: 1021-8 Citation Subset: IM |
Affiliation:
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School of Medical Technology, Zhenjiang Key Institute of Clinical Laboratory Medicine, Jiangsu 212001, PR China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acid Phosphatase
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biosynthesis,
genetics Cell Cycle Proteins / biosynthesis*, genetics Cell Line, Tumor Genes, cdc* Humans Immunohistochemistry Isoenzymes / biosynthesis, genetics Mesenchymal Stem Cells / metabolism, pathology, physiology* Nuclear Proteins / biosynthesis, genetics Oncogenes Proto-Oncogene Proteins / biosynthesis, genetics Proto-Oncogene Proteins c-kit / genetics, metabolism Repressor Proteins / biosynthesis, genetics Telomerase / genetics, metabolism Tumor Markers, Biological / biosynthesis*, genetics |
| Chemical | |
Reg. No./Substance:
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0/Cell Cycle Proteins; 0/Isoenzymes; 0/Nuclear Proteins; 0/Proto-Oncogene Proteins; 0/Repressor Proteins; 0/Tumor Markers, Biological; 138791-04-5/BMI1 protein, human; EC 2.7.10.1/Proto-Oncogene Proteins c-kit; EC 2.7.7.49/Telomerase; EC 3.1.3.-/tartrate-resistant acid phosphatase; EC 3.1.3.2/Acid Phosphatase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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