Tags

Type your tag names separated by a space and hit enter

Prevention of cytokine-induced apoptosis by insulin-like growth factor-I is independent of cell adhesion molecules in HT29-D4 colon carcinoma cells-evidence for a NF-kappaB-dependent survival mechanism.
Cell Death Differ. 2002 Jul; 9(7):768-79.CD

Abstract

We have previously established that insulin-like growth factor (IGF)-I, -II and insulin exert a strong protective effect against tumor necrosis factor-alpha (TNF)-induced apoptosis in interferon-gamma (IFN)-sensitized HT29-D4 human colon carcinoma cells. In this study, we report that this effect was still operative when cells were cultured in the absence of integrin- and E-cadherin-mediated cell-extracellular matrix and cell-cell interactions. In this model, IGF-I did not activate the focal adhesion kinase, whereas it induced tyrosine phosphorylation of the insulin receptor substrate-1 and activation of the extracellular signal-related kinase 1 and 2, p38, phosphatidylinositol 3'-kinase and protein kinase B/Akt. However, the use of specific inhibitors indicated that these pathways did not play a role in the adhesion-independent IGF-I anti-apoptotic signal. In contrast, inhibition of the NF-kappaB activation induced a complete reversal of the IGF-I anchorage-independent protective effect. Correspondingly, IGF-I markedly enhanced the TNF- and IFN/TNF-induced NF-kappaB-dependent interleukin-8 production. Our results provide evidence that IGF-I induces resistance against cytokine-induced cell death even in the absence of cell adhesion-mediated signaling. NF-kappaB appears to be a key mediator of this anti-apoptotic effect that should contribute to the resistance of colon cancer cells to immune-destruction during metastasis.

Authors+Show Affiliations

UMR CNRS 6032, Facultés de Médecine et de Pharmacie, Université de la Méditerranée, Marseille, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12058282

Citation

Garrouste, F, et al. "Prevention of Cytokine-induced Apoptosis By Insulin-like Growth factor-I Is Independent of Cell Adhesion Molecules in HT29-D4 Colon Carcinoma Cells-evidence for a NF-kappaB-dependent Survival Mechanism." Cell Death and Differentiation, vol. 9, no. 7, 2002, pp. 768-79.
Garrouste F, Remacle-Bonnet M, Fauriat C, et al. Prevention of cytokine-induced apoptosis by insulin-like growth factor-I is independent of cell adhesion molecules in HT29-D4 colon carcinoma cells-evidence for a NF-kappaB-dependent survival mechanism. Cell Death Differ. 2002;9(7):768-79.
Garrouste, F., Remacle-Bonnet, M., Fauriat, C., Marvaldi, J., Luis, J., & Pommier, G. (2002). Prevention of cytokine-induced apoptosis by insulin-like growth factor-I is independent of cell adhesion molecules in HT29-D4 colon carcinoma cells-evidence for a NF-kappaB-dependent survival mechanism. Cell Death and Differentiation, 9(7), 768-79.
Garrouste F, et al. Prevention of Cytokine-induced Apoptosis By Insulin-like Growth factor-I Is Independent of Cell Adhesion Molecules in HT29-D4 Colon Carcinoma Cells-evidence for a NF-kappaB-dependent Survival Mechanism. Cell Death Differ. 2002;9(7):768-79. PubMed PMID: 12058282.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prevention of cytokine-induced apoptosis by insulin-like growth factor-I is independent of cell adhesion molecules in HT29-D4 colon carcinoma cells-evidence for a NF-kappaB-dependent survival mechanism. AU - Garrouste,F, AU - Remacle-Bonnet,M, AU - Fauriat,C, AU - Marvaldi,J, AU - Luis,J, AU - Pommier,G, PY - 2001/07/17/received PY - 2001/12/13/revised PY - 2002/01/10/accepted PY - 2002/6/12/pubmed PY - 2003/1/15/medline PY - 2002/6/12/entrez SP - 768 EP - 79 JF - Cell death and differentiation JO - Cell Death Differ VL - 9 IS - 7 N2 - We have previously established that insulin-like growth factor (IGF)-I, -II and insulin exert a strong protective effect against tumor necrosis factor-alpha (TNF)-induced apoptosis in interferon-gamma (IFN)-sensitized HT29-D4 human colon carcinoma cells. In this study, we report that this effect was still operative when cells were cultured in the absence of integrin- and E-cadherin-mediated cell-extracellular matrix and cell-cell interactions. In this model, IGF-I did not activate the focal adhesion kinase, whereas it induced tyrosine phosphorylation of the insulin receptor substrate-1 and activation of the extracellular signal-related kinase 1 and 2, p38, phosphatidylinositol 3'-kinase and protein kinase B/Akt. However, the use of specific inhibitors indicated that these pathways did not play a role in the adhesion-independent IGF-I anti-apoptotic signal. In contrast, inhibition of the NF-kappaB activation induced a complete reversal of the IGF-I anchorage-independent protective effect. Correspondingly, IGF-I markedly enhanced the TNF- and IFN/TNF-induced NF-kappaB-dependent interleukin-8 production. Our results provide evidence that IGF-I induces resistance against cytokine-induced cell death even in the absence of cell adhesion-mediated signaling. NF-kappaB appears to be a key mediator of this anti-apoptotic effect that should contribute to the resistance of colon cancer cells to immune-destruction during metastasis. SN - 1350-9047 UR - https://www.unboundmedicine.com/medline/citation/12058282/Prevention_of_cytokine_induced_apoptosis_by_insulin_like_growth_factor_I_is_independent_of_cell_adhesion_molecules_in_HT29_D4_colon_carcinoma_cells_evidence_for_a_NF_kappaB_dependent_survival_mechanism_ L2 - https://doi.org/10.1038/sj.cdd.4401022 DB - PRIME DP - Unbound Medicine ER -