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  -