Abstract
Apoptosis is a mode of cell death with characteristic structural features. These appear to result from a set of discrete cellular events that are regulated by gene expression. Oncogenesis and oncosuppressor genes are involved in this regulation. The role of c-myc is of particular interest, as it can act as a bivalent regulator, determining either cell proliferation or apoptosis, depending on whether free movement around the cell cycle is supported (by growth factors) or is limited by growth factor deprivation or treatment with other cycle-blocking agents. In vivo, c-myc expression may be associated with a 'high-turnover' state in which cell proliferation and apoptosis co-exist. Certain other oncogenes (e.g. ras, bcl-2) rescue cells from susceptibility to apoptosis and so convert this high-turnover state into rapid population expansion. One role of the oncosuppressor gene p53 may be to initiate apoptosis by causing G 1/S arrest in cells expressing c-myc. Some aspects of resistance and sensitivity to chemotherapeutic agents can be explained on the basis of movement between the population-expansion and the high-turnover states, perhaps through modulation of the expression of these and other genes.
Highlights
The morphological changes in apoptosis have been extensively reviewed elsewhere (Kerr et al, 1972; Wyllie et al, 1980; Kerr et al, 1987; Arends et al, 1990)
There is a cascade-like induction of c-fos, c-myc and hsp-70 in regressing prostate, for example (Buttyan et al, 1988), and TGFP1 is induced during regression of a hormone-sensitive breast carcinoma cell line (Kyprianou et al, 1991b), but it is difficult from experiments of this type to be certain that the new transcripts are integral to apoptosis as opposed to other stress responses
Expression of c-myc is of particular interest, as it seems to determine either continuous proliferation or apoptosis, depending on the availability of critical growth factors (Evan et al, 1992)
Summary
The morphological changes in apoptosis have been extensively reviewed elsewhere (Kerr et al, 1972; Wyllie et al, 1980; Kerr et al, 1987; Arends et al, 1990). There is a cascade-like induction of c-fos, c-myc and hsp-70 in regressing prostate, for example (Buttyan et al, 1988), and TGFP1 is induced during regression of a hormone-sensitive breast carcinoma cell line (Kyprianou et al, 1991b), but it is difficult from experiments of this type to be certain that the new transcripts are integral to apoptosis as opposed to other (perhaps abortive) stress responses.
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