title: Histological type of oncogenity and expression of cell cycle genes in tumor cells from human mesenchymal stem cells.
abstract: 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.
authors.affiliation: School of Medical Technology, Zhenjiang Key Institute of Clinical Laboratory Medicine, Jiangsu 212001, PR China.
authors.forename: Runqiu
authors.initials: R
authors.lastname: Jiang
authors.forename: Wenrong
authors.initials: W
authors.lastname: Xu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhu
authors.forename: Miao
authors.initials: M
authors.lastname: Chen
authors.forename: Hui
authors.initials: H
authors.lastname: Qian
authors.forename: Chun
authors.initials: C
authors.lastname: Qiao
authors.forename: Huan
authors.initials: H
authors.lastname: Yang
authors.forename: Xingzhong
authors.initials: X
authors.lastname: Wang
authors.forename: Yongchang
authors.initials: Y
authors.lastname: Chen
mesh_terms: D000135:Acid Phosphatase / Q000096:biosynthesis / Q000235:genetics; D014408:Biomarkers, Tumor / Q000096:biosynthesis* / Q000235:genetics; D018797:Cell Cycle Proteins / Q000096:biosynthesis* / Q000235:genetics; D045744:Cell Line, Tumor; D018816:Genes, cdc; D006801:Humans; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000096:biosynthesis / Q000235:genetics; D059630:Mesenchymal Stem Cells / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D009687:Nuclear Proteins / Q000096:biosynthesis / Q000235:genetics; D009857:Oncogenes; D063150:Polycomb Repressive Complex 1; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics; D019009:Proto-Oncogene Proteins c-kit / Q000235:genetics / Q000378:metabolism; D012097:Repressor Proteins / Q000096:biosynthesis / Q000235:genetics; D000071681:Tartrate-Resistant Acid Phosphatase; D019098:Telomerase / Q000235:genetics / Q000378:metabolism
chemical_list: C069077:BMI1 protein, human; D014408:Biomarkers, Tumor; D018797:Cell Cycle Proteins; D007527:Isoenzymes; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D063150:Polycomb Repressive Complex 1; D019009:Proto-Oncogene Proteins c-kit; D019098:Telomerase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase