Abstract:
:Neoplastic transformation is characterised by an imbalance in favour of cell growth over programmed cell death (apoptosis). The tumour-suppressor gene p53, responsible for maintaining cell-cycle control, is mutated in the majority of human cancers. Loss of function of the target genes of p53 are therefore important in tumourigenesis. One such target gene is the insulin-like growth factor binding protein-3 (IGFBP-3), an extracellular protein responsible for the carriage of IGF-I but which can act independently of IGF-I, inhibiting cell growth and enhancing apoptosis. Using the KYSE 190 oesophageal carcinoma cell line, we have demonstrated that IGFBP-3 alone has no effect on cell growth or cell survival. However, it significantly enhanced apoptosis, with a 67% increase in the pre-G1 peak on flow cytometry following UV irradiation. The increase in p53 was enhanced and prolonged when cells are stressed in the presence of IGFBP-3. These data suggest an autocrine/paracrine feedback loop exists between IGFBP-3 and p53, which may provide the social control necessary to maintain normal tissue homeostasis.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Hollowood AD,Lai T,Perks CM,Newcomb PV,Alderson D,Holly JMkeywords:
subject
Has Abstractpub_date
2000-11-01 00:00:00pages
336-41issue
3eissn
0020-7136issn
1097-0215pii
10.1002/1097-0215(20001101)88:3<336::AID-IJC3>3.0.journal_volume
88pub_type
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