Abstract
Autocrine growth factor secretion has classically been considered as a mechanism by which tumour cells achieve autonomous growth. However, there is now considerable evidence that autocrine circuits operate in the growth regulation of normal adult tissues. Here we consider the possible advantages to the normal epithelial cell of utilising such an external growth factor circuit and suggest that autocrine growth factor secretion, when viewed in a multicellular context, could paradoxically form part of a mechanism for preventing tumour development.
Highlights
The autocrine hypothesis of growth regulation was first proposed to account for growth factor independence in tumours (Sporn and Todaro. 1980), and much evidence has accumulated to support this idea (Sporn and Roberts, 1985; Cross and Dexter, 1991; Daughaday and Deuel, 1991)
Summary Autocrine growth factor secretion has classically been considered as a mechanism by which tumour cells achieve autonomous growth
There is considerable evidence that autocrine circuits operate in the growth regulation of normal adult tissues
Summary
The autocrine hypothesis of growth regulation was first proposed to account for growth factor independence in tumours (Sporn and Todaro. 1980), and much evidence has accumulated to support this idea (Sporn and Roberts, 1985; Cross and Dexter, 1991; Daughaday and Deuel, 1991). Further studies have demonstrated that TSH stimulates IGFI secretion (Tode et al, 1989) and reduces specific IGF-Ibinding protein (Wang et al, 1990), both of which would be predicted to increase local free IGF-I concentration Together these data suggest that IGF-I plays a key physiological role in synergising with the TSH stimulus to promote thyrocyte growth and that part of this mechanism involves the induction of an IGF-I autocrine circuit by TSH in the target tissue. There is compelling evidence that aberrant production of IGF-I is involved in the genesis of thyroid tumours (follicular adenomas), in many cases as a result of the oncogenic activation of the ras family of signal transduction proteins (Lemoine et al, 1989; Suarez et al, 1990; Dawson et al, 1995) These finding are in accordance with a general shift in emphasis over recent years, from an endocrine to a paracrine or autocrine role for IGF-I in growth regulation
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