TY - JOUR AV - public A1 - Yang, SY A1 - Bolvin, C A1 - Sales, KM A1 - Fuller, B A1 - Seifalian, AM A1 - Winslet, MC SN - 1471-2407 N2 - Background: Colorectal cancer is the third most common cancer in the western world. Chemotherapy is often ineffective to treat the advanced colorectal cancers due to the chemoresistance. A major contributor to chemo-resistance is tumour-derived inhibition or avoidance of apoptosis. Insulin-like growth factor I (IGF-I) has been known to play a prominent role in colorectal cancer development and progression. The role of IGF-I in cancer cell apoptosis is not completely understood.Methods: Using three colorectal cancer cell lines and one muscle cell line, associations between IGF-I and activities of caspase 3/7, 8 and 9 have been examined; the role of insulin-like growth factor I receptor (IGF-IR) in the caspase activation has been investigated.Results: The results show that exogenous IGF-I significantly increases activity of caspases 3/7, 8 and 9 in all cell lines used; blocking IGF-I receptor reduce IGF-I-induced caspase activation. Further studies demonstrate that IGF-I induced caspase activation does not result in cell death. This is the first report to show that while IGF-I activates caspases 3/7, 8 and 9 it does not cause colorectal cancer cell death.Conclusion: The study suggests that caspase activation is not synonymous with apoptosis and that activation of caspases may not necessarily induce cell death. KW - ALPHA-INDUCED APOPTOSIS KW - COLON-CARCINOMA CELLS KW - GROWTH-FACTORS KW - TRANSFORMING ACTIVITIES KW - GENE-EXPRESSION KW - RECEPTOR KW - DIFFERENTIATION KW - 5-FLUOROURACIL KW - PROLIFERATION KW - PATHWAYS PB - BIOMED CENTRAL LTD JF - BMC Cancer VL - 9 TI - IGF-I activates caspases 3/7, 8 and 9 but does not induce cell death in colorectal cancer cells N1 - © 2009 Yang et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ID - discovery139906 UR - http://dx.doi.org/10.1186/1471-2407-9-158 Y1 - 2009/05/21/ ER -