Literature DB >> 29311337

Phenotypic selection as the biological mode of epigenetic conversion and reversion in cell transformation.

Harry Rubin1, Andrew L Rubin2.   

Abstract

Exposure of certain cell lines to methylcholanthrene, X-rays, or physiological growth constraint leads to preneoplastic transformation in all or most of the treated cells. After attaining confluence, a fraction in those cells progress to full transformation, as evidenced by their ability to form discrete foci distinguishable from the surrounding cells by virtue of their higher density. Transformation induced by suspension in agar, an even stronger growth-selective condition than confluence, is reminiscent of all but the final differentiated stage of a normal developmental process, epithelial-mesenchymal transition. Changes associated with transformation are not restricted to focus-forming cells, as the permissiveness for focus formation provided by confluent cells surrounding transformed foci is greater than that of nonselected cells. The neoplastic process can also be reversed in culture. Transformed cells passaged at low density in high serum revert to normal morphology and growth behavior in vitro and lose the capacity for tumor formation in vivo. We propose that transformation and its reversal are driven by a process of phenotypic selection that involves entire heterogeneous populations of cells responding to microenvironmental changes. Because of the involvement of whole cell populations, we view this process as fundamentally adaptive and epigenetic in nature.

Entities:  

Keywords:  epigenetics; malignant transformation; phenotypic selection; saturation density

Mesh:

Year:  2018        PMID: 29311337      PMCID: PMC5789940          DOI: 10.1073/pnas.1717299115

Source DB:  PubMed          Journal:  Proc Natl Acad Sci U S A        ISSN: 0027-8424            Impact factor:   11.205


  38 in total

Review 1.  A CLONAL SELECTION THEORY OF CHEMICAL CARCINOGENESIS.

Authors:  R T PREHN
Journal:  J Natl Cancer Inst       Date:  1964-01       Impact factor: 13.506

2.  Physiological induction and reversal of focus formation and tumorigenicity in NIH 3T3 cells.

Authors:  A L Rubin; P Arnstein; H Rubin
Journal:  Proc Natl Acad Sci U S A       Date:  1990-12       Impact factor: 11.205

3.  Reversion of properties in cells transformed by polyoma virus.

Authors:  Z Rabinowitz; L Sachs
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4.  Chromosomal mechanism for the induction of reversion in transformed cells.

Authors:  N Bloch-Shtacher; Z Rabinowitz; L Sachs
Journal:  Int J Cancer       Date:  1972-05-15       Impact factor: 7.396

5.  Relationship between x-ray exposure and malignant transformation in C3H 10T1/2 cells.

Authors:  A R Kennedy; M Fox; G Murphy; J B Little
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Journal:  Proc Natl Acad Sci U S A       Date:  1989-03       Impact factor: 11.205

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