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We are analyzing https://link.springer.com/article/10.1007/bf01233159.

Title:
Recovery of the missing tumorigenicity in mitochondrial DNA-less HeLa cells by introduction of mitochondrial DNA from normal human cells | Somatic Cell and Molecular Genetics
Description:
The role of mitochondrial DNA (mtDNA) in the expression of the transformed phenotype was examined using mtDNA-less HeLa cells. Complete depletion of mtDNA and its products in the mtDNA-less HeLa cell line, EB8, was confirmed by Southern blot analysis and by [35S]methionine labeling of mitochondrially synthesized polypeptides. The tumorigenicity of the EB8 cells was assayed by inoculation of 1Γ—107 cells subcutaneously into the backs of nude mice. The results showed that the tumorigenicity of HeLa cells was lost in good correspondence with the loss of mtDNA. However, the growth of EB8 cells in culture was very poor compared with that of HeLa cells, indicating that the apparent loss of tumorigenicity in EB8 cells could possibly be due to poor growth of the cells. Introduction of mtDNA from normal human fibroblasts into EB8 cells restored both the missing tumorigenicity and growth of the EB8 cells. These observations could be interpreted to show that mtDNA is required for expression of tumorigenicity, but that mutational changes of the mtDNA are not required for modulation of the phenotype in our experiments.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Education
  • Telecommunications

Content Management System {πŸ“}

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Custom-built

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Traffic Estimate {πŸ“ˆ}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

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Keywords {πŸ”}

google, scholar, pubmed, cells, cancer, res, cell, article, hayashi, tumorigenicity, hela, research, mitochondrial, dna, human, mtdna, access, privacy, cookies, content, publish, search, nonaka, growth, shay, analysis, data, information, log, journal, missing, introduction, normal, takemitsu, expression, products, open, discover, vol, nature, science, werbin, yonekawa, tagashira, van, genet, download, springer, optional, personal,

Topics {βœ’οΈ}

month download article/chapter southern blot analysis article somatic cell related subjects [35s]methionine labeling hela cell line normal human fibroblasts normal human cells privacy choices/manage cookies full article pdf experimental tumor research mitochondrial dna mitochondrial dna check access instant access european economic area mitochondrially synthesized polypeptides transcription factor eb conditions privacy policy article hayashi accepting optional cookies cell res eb8 cells restored main content log cell biol journal finder publish usage analysis van dongen ultrastructural research article log hela cells article cite privacy policy personal data national institute national center books a cancer res optional cookies manage preferences takemitsu eb8 cells 1Γ—107 cells subcutaneously data protection essential cookies cookies skip subscription content similar content institution subscribe journal publish

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Recovery of the missing tumorigenicity in mitochondrial DNA-less HeLa cells by introduction of mitochondrial DNA from normal human cells
         description:The role of mitochondrial DNA (mtDNA) in the expression of the transformed phenotype was examined using mtDNA-less HeLa cells. Complete depletion of mtDNA and its products in the mtDNA-less HeLa cell line, EB8, was confirmed by Southern blot analysis and by [35S]methionine labeling of mitochondrially synthesized polypeptides. The tumorigenicity of the EB8 cells was assayed by inoculation of 1Γ—107 cells subcutaneously into the backs of nude mice. The results showed that the tumorigenicity of HeLa cells was lost in good correspondence with the loss of mtDNA. However, the growth of EB8 cells in culture was very poor compared with that of HeLa cells, indicating that the apparent loss of tumorigenicity in EB8 cells could possibly be due to poor growth of the cells. Introduction of mtDNA from normal human fibroblasts into EB8 cells restored both the missing tumorigenicity and growth of the EB8 cells. These observations could be interpreted to show that mtDNA is required for expression of tumorigenicity, but that mutational changes of the mtDNA are not required for modulation of the phenotype in our experiments.
         datePublished:
         dateModified:
         pageStart:123
         pageEnd:129
         sameAs:https://doi.org/10.1007/BF01233159
         keywords:
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            Polypeptide
            Methionine
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            Plant Sciences
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               name:Jun-Ichi Hayashi
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                     name:Saitama Cancer Center Research Institute
                     address:
                        name:Department of Biochemistry, Saitama Cancer Center Research Institute, Saitama, Japan
                        type:PostalAddress
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               name:Masakazu Takemitsu
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                     name:National Center of Neurology and Psychiatry
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                        name:Division of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
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      headline:Recovery of the missing tumorigenicity in mitochondrial DNA-less HeLa cells by introduction of mitochondrial DNA from normal human cells
      description:The role of mitochondrial DNA (mtDNA) in the expression of the transformed phenotype was examined using mtDNA-less HeLa cells. Complete depletion of mtDNA and its products in the mtDNA-less HeLa cell line, EB8, was confirmed by Southern blot analysis and by [35S]methionine labeling of mitochondrially synthesized polypeptides. The tumorigenicity of the EB8 cells was assayed by inoculation of 1Γ—107 cells subcutaneously into the backs of nude mice. The results showed that the tumorigenicity of HeLa cells was lost in good correspondence with the loss of mtDNA. However, the growth of EB8 cells in culture was very poor compared with that of HeLa cells, indicating that the apparent loss of tumorigenicity in EB8 cells could possibly be due to poor growth of the cells. Introduction of mtDNA from normal human fibroblasts into EB8 cells restored both the missing tumorigenicity and growth of the EB8 cells. These observations could be interpreted to show that mtDNA is required for expression of tumorigenicity, but that mutational changes of the mtDNA are not required for modulation of the phenotype in our experiments.
      datePublished:
      dateModified:
      pageStart:123
      pageEnd:129
      sameAs:https://doi.org/10.1007/BF01233159
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         Animal Anatomy / Morphology / Histology
         Plant Sciences
         Biochemistry
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                     name:Department of Biochemistry, Saitama Cancer Center Research Institute, Saitama, Japan
                     type:PostalAddress
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            name:Masakazu Takemitsu
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                  name:National Center of Neurology and Psychiatry
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                     name:Division of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
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                  name:National Center of Neurology and Psychiatry
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               name:Division of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
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            name:National Center of Neurology and Psychiatry
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               name:Division of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
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      name:Department of Biochemistry, Saitama Cancer Center Research Institute, Saitama, Japan
      name:Division of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
      name:Division of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
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