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  • 1
    Electronic Resource
    Electronic Resource
    cDNA Cloning of an Extraembryonic Endodermal Intermediate Filament Protein (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 455 (1985), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1985.tb50451.x
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  • 2
    Electronic Resource
    Electronic Resource
    Role of intermediate filaments in migration, invasion and metastasis (1996)
    Springer
    Cancer and metastasis reviews 15 (1996), S. 507-525 
    Details
    ISSN: 1573-7233
    Keywords: keratins ; vimentin ; intermediate filaments ; cancer ; invasion ; metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The expression of intermediate filament proteins is remarkably tissue-specific which suggests that the intermediate filament (IF) type(s) present in cells is somehow related to their biological function. However, in some cancers-particularly malignant melanoma and breast carcinoma, there is a strong indication that vimentin and keratin IFs are coexpressed, thus presenting as a dedifferentiated or interconverted (between epithelial and mesenchymal) phenotype. In this review, twoin vitro models are presented which recapitulate the interconverted phenotype in human melanoma and breast carcinoma, and allow, for the first time, unique observations to be made with respect to the role of IFs in cancer progression. These studies have provided direct evidence linking overexpression of keratin IFs in human melanoma with increased migratory and invasive activityin vitro, which can be down-regulated by substituting dominant-negative keratin mutants. Overexpression of vimentin IFs in the breast carcinoma model leads to augmentation of motility and invasivenessin vitro, which can be transiently down-regulated by treatment with antisense oligonucleotides to vimentin. Additional experimental evidence suggests that the mechanism(s) responsible for the differential expression of metastatic properties associated with the interconverted phenotype rest(s) in the unique interaction, either direct or indirect, of IFs with specific integrins interacting with the extracellular matrix. In this review, we discuss the observations derived from the human melanoma and breast carcinoma models to address the hypothesis that the ability to coexpress vimentin and keratins confers a selective advantage to tumor cells in their interpretation of and response to signaling cues from the extracellular matrix. The ramifications of these observations are discussed with respect to the patholophysiology of the respectivein situ tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00054016
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  • 3
    Electronic Resource
    Electronic Resource
    Structural and biological consequences of increased vimentin expression in simple epithelial cell types (1995)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 32 (1995), S. 10-25 
    Details
    ISSN: 0886-1544
    Keywords: desmosomes ; embryonal carcinoma ; epithelia ; intermediate filaments ; keratins ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Cytoskeletal intermediate filaments (IFs) constitute a diverse family of proteins whose members are expressed in tissue-specific patterns. Although vimentin IFs are normally restricted to mesenchyme, a variety of cell types express vimentin alone or together with cell-specific IFs during growth, differentiation, and neoplasia. In this study, we have investigated the influence of increased vimentin expression on the simple epithelial cell phenotype. An expression vector encoding a human vimentin cDNA was transfected into the murine HR9 endoderm and F9 embryonal carcinoma cell lines, which serve as models for early extraembryonic epithelial differentiation. Stable clones that expressed varying levels of the human vimentin were characterized by immunofluorescence and biochemical analysis. A relatively high level of vimentin expression in HR9 and differentiated F9 epithelial cells resulted in aberrant vimentin structures with a co-collapss of keratin K8/K18 filaments and lowered amounts of keratin protein. In F9 epithelial cells, the desmosomal proteins DP I/II did not appear to localize to cell surface desmosomes but rather co-aggregated with the perturbed IFs. Although overall cell morphology was not dramatically altered, individual nuclei were distorted by excess intracellular vimentin. Furthermore, cell proliferation as well as the cell spreading response time were slowed. There appears to be a threshold effect regarding overall vimentin levels as cells that expressed lower amounts of the human vimentin exhibited no obvious structural nor biological effects. Our results demonstrate that wild-type vimentin can act as a “mutant” protein when present at high intracellular levels, inducing a variety of phenotypic changes. © 1995 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970320103
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  • 4
    Electronic Resource
    Electronic Resource
    Karyology and tumorigenicity of a Simian virus 40-transformed chinese hamster cell cloneThis work was supported in part by Grants CA-16130 and CA-15823 from the National Cancer Institute. (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 98 (1979), S. 443-450 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A pseudodiploid clone of Chinese hamster cells transformed in vitro with Simian virus 40 (SV40) was isolated from soft agar and injected into nude mice through three successive passages with a short in vitro cultivation between each animal inoculation. The original clone and the three subsequent tumor populations were characterized in regard to SV40 T antigen staining, modal chromosome number, and Giemsa-banded karyotype. All tumor cell lines maintained the pseudodiploid mode, as well as the positive SV40 T antigen staining. Nonrandom chromosomal changes included loss of one of the X chromosomes, additions of abnormal variants of chromosomes No. 1 and No. 2, the appearance of unidentified marker chromosomes, and the loss of autosomes No. 5, No. 6, and No. 11. The deletion of one of the X chromosomes occurred with about the same frequency in all cell lines. Additions of abnormal chromosomes No. 1 and No. 2 tended to recur more often in the tumor cell lines than in the original clone. The appearance of marker chromosomes, as well as the loss of autosomes No. 5, No. 6, and No. 11 demonstrated a correlation with tumorigenicity. Yet, the three successive passages of the cells through the animal did not select for a tumor population with a single, homogeneous karyotype.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040980302
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  • 5
    Electronic Resource
    Electronic Resource
    The interaction of polyoma virus with F9 embryonal carcinoma cells and chemically induced differentiated progeny: Fate of the viral DNA and expression of viral antigens (1982)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 113 (1982), S. 69-83 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Murine embryonal carcinoma (EC) cells fail to express viral T antigen following infection with polyoma (Py) virus, while some differentiated derivatives are fully susceptible to viral infection. The block to expression in EC cells apparently occurs after adsorption and penetration but prior to the synthesis of early viral proteins. The F9 EC cell line was employed to further investigate the failure of Py gene expression in EC cells as well as the viral susceptibility of certain differentiated cell types. F9 cultures treated with retinoic acid (RA) or RA in combination with dibutyryl cAMP (dBcAMP) are quantitatively induced to differentiate to endodermal cell types. When the fate of the viral DNA was examined in F9 EC cells, free viral DNA was observed early after infection but was eventually lost with continued cell growth. Cultures induced to differentiate in the presence of RA demonstrated limited viral susceptibility which increased with prolonged RA exposure. Polyoma sensitivity did not directly parallel basement membrane antigen production, a marker used to distinguish this differentiated endodermal cell type. Viral gene expression could be obtained if Py DNA was introduced into the cells prior to RA induction. In contrast, the endodermal progeny derived from a dual treatment with RA plus dBcAMP appeared highly refractory to Py infection.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041130512
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