A possible role of cell membranes in regulation of cell division and malignant transformation

P M BHARGAVA & S A CHANDANI

Published in: In Membrane Dynamics and Transport of Normal and Tumour Cells (Ed. S. Damjanovich) (Hungarian Academy of Sciences), 1984, pp.253-258.

Abstract:

It was recently proposed by one of us (Bhargava, 1974, 1975, 1977) that a resting cell is a resting cell because it is unable to take up essential nutrients at rates obtained in – and, apparently, necessary for – dividing cells. It was pointed out that all cells in which a true resting state is obtained are, without exception, auxotrophic for a number of carbon-containing nutrients. It was proposed that, in resting cells, only one of the two postulated functionally different transport sites for essential nutrients is open. When this site (Site A) operates at its maximal velocity, the uptake is just sufficient to take care of the requirements of the resting state. The second site (Site B) was proposed to be closed in resting cells through the interaction of a transport-inhibitory protein (made inside in the cell for translocation outside, and called I) with its receptor on the cell membrane. The sites through which the-transport machinery operates, irrespective of the mechanism of uptake, were suggested to be spatially linked to the site for the receptor for I. Thus, I+ phenotype would mean that Sites B are closed and the cell would be a resting cell, and I– phenotype will imply that Sites B are open and, therefore, the cell can go-through the division cycle.

It was further suggested that mitogens act by making the cell I-, for example, by binding to a site (also spatially linked to the receptor site for I) on the cell membrane in such a way that, following an allosteric transition, I can no longer bind to its own receptors. Malignancy, in terms of the model would be the consequence of a situation where cells are not only phenotypically I-, but also no longer possess the ability to revert back to the I+ state. Such a situation could arise as a result of, for example, (a)-mutation in the gene for I or for its receptor; (b) introduction of new information in the cell, say, through an oncogenic virus, which leads to the synthesis of a protein that gets associated with the cell membrane in such a way that I can no longer bind to its own receptor; or (c) mutation in the regulatory or the structural part of a host gene (e.g., the cellular counterpart of a viral oncogene) which codes – either in its normal or in its mutated form – for a product which migrates to the cell membrane and performs the same function as suggested above for a mitogen.

HOW TO CITE

A possible role of cell membranes in regulation of cell division and malignant transformation. P M BHARGAVA & S A CHANDANI. In Membrane Dynamics and Transport of Normal and Tumour Cells (Ed. S. Damjanovich) (Hungarian Academy of Sciences), 1984, pp.253-258.

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