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  • 1
    Electronic Resource
    Electronic Resource
    Immortalization of human dental papilla, dental pulp, periodontal ligament cells and gingival fibroblasts by telomerase reverse transcriptase (2004)
    Oxford, UK : Munksgaard International Publishers
    Journal of oral pathology & medicine 33 (2004), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Human telomerase reverse transcriptase (hTERT) is catalytic subunit of human telomerase.Methods:  We studied the immortalization of a series of human dental and periodontal cells by ectopic expression of hTERT and co-expression of hTERT with human papilloma virus 16 (HPV16) or simian virus 40 (SV40). Differentiation abilities of the established cell lines were studied in terms of the mineralized matrix formation and gene expression.Results:  We established immortalized gingival fibroblasts by hTERT, dental papilla and periodontal ligament cells by hTERT and HPV16, and pulp cells by hTERT and SV40. The papilla and pulp cells showed mineralization and dentin sialophosphoprotein (DSPP) expression when cultured in the presence of β-glycerophosphate. The immortalized periodontal ligament cells did not show mineralization or DSPP expression, although expressions of alkaline phosphatase, osteopontin and osteocalcin were detected.Conclusions:  These cell lines will be useful tools for studying the repair and regeneration of dental and periodontal tissues and various diseases including odontogenic tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.2004.00228.x
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  • 2
    Electronic Resource
    Electronic Resource
    Overexpression of bcl-2 protein inhibits terminal differentiation of oral keratinocytes in vitro (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 27 (1998), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Harada H, Mitsuyasu T, Seta Y. Maruoka Y, Toyoshima K, Yasumoto S: Overexpression of bcl-2 protein inhibits terminal differentiation of oral keratinocytes in vitro. J Oral Pathol Med 1998; 27: 11–7. © Munksgaard, 1998.The bcl-2 proto-oncogene is a known inhibitor of apoptosis; in normal human stratified squamous epithelium, its expression is restricted to the basal cell layer. To investigate the functional role of bcl-2 protein in the process of differentiation of oral keratinocytes, bcl-2 expression vector was transfected into SCC-25 cells, which normally undergo squamous cell differentiation in vitro while expressing specific differentiation markers, e.g., keratin 10/11 and involucrin. In bcl-2 transfected SCC-25 cells, the expression of these differentiation markers was markedly suppressed. The bcl-2 proto-oncogene may play a critical role in opposing the commitment to terminal differentiation and apoptosis of oral keratinocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1998.tb02084.x
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  • 3
    Electronic Resource
    Electronic Resource
    Monoclonal antibody G6K12 specific for membrane-associated differentiation marker of human stratified squamous epithelia and squamous cell carcinoma (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 22 (1993), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Monoclonal antibody (G6KI2) specific for differentiated keratinocytes was developed using in vitro immunization against the SCC-25 cell line. G6K 12 only recognized stratified portions of cultured SCC-25 cells. Immunohistochemical examination using normal human oral mucosa showed that specific G6K12-reactivity was limited to the lower spinous-cell layers, while this antibody weakly bound to cells in basal-cell layers as well as in the upper spinous, granular and cornified-cell layers. G6KI2 was also reactive to keratinocytes in most moderatel-y- and well-differentiated SCC tissues. Immunoelectron microscopic examination further demonstrated that the G6K. 12-immunoreactive area was at the outer surface of the entire plasma membrane, including the microvilli of stratified SCC-25. G6KI2-binding was reduced 50% by the treatment of native cells with glycoendoceramidase for 2 h. These results suggest that G6K12 recognizes a plasma membrane-anchored glycoconjugate which is specific for differentiated keratinocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1993.tb01047.x
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  • 4
    Electronic Resource
    Electronic Resource
    Establishment of ameloblastoma cell line, AM-1 (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 27 (1998), S. 0 
    Details
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Ameloblastomas are slowly growing, locally invasive neoplasms with a potentially destructive behaviour. The molecular mechanisms that regulate the cell growth and invasion of ameloblastoma cells are unknown. Because ameloblastoma cells placed in culture have a very limited lifespan, the establishment of immortalized clones of ameloblastoma cells would aid its study. We produced an immortalized ameloblastoma cell line (AM-1) using human papillomavirus type-16. This cell line maintains epithelial cell morphology and expresses cytokeratins K8, K14, K18, K19. Furthermore, bcl-2 protein, which prevents apoptosis, is expressed. We investigated the behaviour of these cells on a collagen matrix in vitro. These cells grew in a monolayer over foci of collagen degradation and could invade the collagen gel at such sites. Since the behavior of cell line AM-1 mimics the behavior of ameloblastoma in vivo, it may be a valuable model for the study of these neoplasms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0714.1998.tb01943.x
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  • 5
    Electronic Resource
    Electronic Resource
    A major transcript of human papillomavirus type 16 in transformed NIH 3T3 cells contains polycistronic mRNA encoding E7, E5, and E1^E4 fusion gene (1990)
    Springer
    Virus genes 3 (1990), S. 221-233 
    Details
    ISSN: 1572-994X
    Keywords: HPV 16 ; transformation ; NIH 3T3 cells ; polycistronic mRNA ; cDNA cloning ; sequencing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have cloned cDNA of the major 1.8 kb mRNA from HPV 16-transformed NIH 3T3 cells (PM3T3). The entire nucleotide sequences of this cDNA were determined and compared with prototype HPV 16 genomic DNA sequences. The 5′-end of the cDNA was flanked by approximately 300 bp of cellular sequences, and the 3′-end of the cDNA sequences contained poly A residues following at nt 4230. HPV 16 sequences began at nt 124, downstream of a major viral p97 promoter, within the E6 open reading frame (ORF). The first splice donor site was at nt 226 and the splice acceptor site was at nt 409, suggesting that the E6 gene is inert. Second splice donor and acceptor sites were located at nt 880 and at nt 3357, respectively. This mRNA was thus shown to consist of three exons, resulting in polycistronic mRNA containing three potentially functional virus early genes-E7, E1^E4, and E5-actively transcribed in the transformant.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00393182
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  • 6
    Electronic Resource
    Electronic Resource
    Induction of the HPV16 enhancer activity byJun-B and c-Fos through cooperation of the promoter-proximal AP-1 site and the epithelial cell type- specific regulatory element in fibroblasts (1996)
    Springer
    Virus genes 13 (1996), S. 45-52 
    Details
    ISSN: 1572-994X
    Keywords: HPV16 ; enhancer ; cell type- specificity ; Jun-B ; c-Fos
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The epithelial cell type- specific enhancer of the human papillomavirus (HPV) type 16 termed the long control region (LCR) carries three AP-1 binding sites. We investigated the roles of the AP-1 sites for transactivation of the LCR byJun-B that may be a cell type specific- transactivator for the HPVs in human fibroblasts in which expression of the endogenousjun-B gene is low. Transient expression ofJun-B alone poorly activated transcriptional activity of the LCR. However, when combined with c-Fos,Jun-B activated the LCR. The promoter-proximal AP-1 site was required for transactivation of the LCR byJun-B:c-Fos, but the site itself was not sufficient for the maximal response. The proposed cell type specific- regulatory element that harbors binding sites for NF1 as well as TEF-1 and PEA3 motifs, but neither other AP-1 sites nor the proximal enhancer region, could augment the transcriptional response of the promoter-proximal AP-1 site toJun-B:c-Fos.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00576977
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  • 7
    Electronic Resource
    Electronic Resource
    Differentiation of the rat myelomonocytic leukemia cell line c-WRT-7 by in vitro culture with the rat bone marrow preadipocyte cell line REC A16 (1993)
    Springer
    Journal of cancer research and clinical oncology 119 (1993), S. 335-341 
    Details
    ISSN: 1432-1335
    Keywords: Differentiation ; Leukemia cell ; Stromal cell ; Colony-stimulating factor ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Differentiation of the rat myelomonocytic leukemia cell line (c-WRT-7) was investigated, by co-culture with a rat embryonic bone marrow preadipose cell line (REC A16). Co-cultivation with REC A16, or with conditioned medium from REC A16 cultures (REC-CM), induced differentiation of c-WRT-7 cells to macrophages. A soluble factor(s) produced by REC A16 appeared to be responsible for the differentiation of c-WRT-7. Because REC-CM was associated with colony-stimulating activity on murine marrow progenitors, c-WRT-7 cells were cultured with various colony-stimulating factors (CSF) and it was found that macrophage CSF (M-CSF) significantly induced differentiation of c-WRT-7. We further demonstrated that both the colonystimulating and differentiation-inducing activities of REC-CM were significantly blocked by anti-M-CSF antiserum. These results suggest that the differentiation of c-WRT-7 is due to M-CSF produced by REC A16. Co-culture of these two cell lines should provide a useful model to study the mechanisms of interaction between leukemia cells and marrow stroma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01208841
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