Tags

Type your tag names separated by a space and hit enter

Requirement of c-Jun NH2-terminal kinase activation in interferon-alpha-induced apoptosis through upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in Daudi B lymphoma cells.
Exp Cell Res. 2005 Oct 15; 310(1):10-21.EC

Abstract

Interferon alpha (IFN-alpha) inhibits growth, at least in part, through induction of apoptosis. However, the molecular mechanisms underlying IFN-alpha-induced apoptosis are not completely understood. In the present study, we found that IFN-alpha induced a sustained activation of c-Jun N-terminal kinase 1 (JNK1), but not extracellular kinases (ERKs), in Daudi B lymphoma cells, as assessed by Western blotting using phospho-specific antibodies. Several lines of evidence support the notion that the IFN-alpha-induced activation of JNK is responsible for IFN-alpha-induced apoptosis, at least in part, through upregulation of TNF-related apoptosis-inducing ligand (TRAIL). First, pretreatment of Daudi cells with a JNK inhibitor reduced IFN-alpha-induced upregulation of TRAIL and loss of mitochondrial membrane potential (DeltaPsim) and annexin-positive cells, which was assessed by flow cytometry. Second, a dominant-negative form of JNK1 (dnJNK1) also reduced these apoptotic events, while a constitutively active form of JNK1, MKK7-JNK1beta, enhanced them. Finally, treatment with IFN-alpha enhanced the promoter activity of the TRAIL gene, which was partially abrogated by either JNK inhibitor or dnJNK1, while it was moderately enhanced by MKK7-JNK1beta. These findings are useful for understanding molecular mechanisms of IFN-alpha-induced apoptosis and also for development of treatment modalities of some tumors with IFN-alpha.

Authors+Show Affiliations

Department of Immunology and Intractable Immunology Research Center, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8402, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16099454

Citation

Yanase, Noriko, et al. "Requirement of c-Jun NH2-terminal Kinase Activation in Interferon-alpha-induced Apoptosis Through Upregulation of Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) in Daudi B Lymphoma Cells." Experimental Cell Research, vol. 310, no. 1, 2005, pp. 10-21.
Yanase N, Hata K, Shimo K, et al. Requirement of c-Jun NH2-terminal kinase activation in interferon-alpha-induced apoptosis through upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in Daudi B lymphoma cells. Exp Cell Res. 2005;310(1):10-21.
Yanase, N., Hata, K., Shimo, K., Hayashida, M., Evers, B. M., & Mizuguchi, J. (2005). Requirement of c-Jun NH2-terminal kinase activation in interferon-alpha-induced apoptosis through upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in Daudi B lymphoma cells. Experimental Cell Research, 310(1), 10-21.
Yanase N, et al. Requirement of c-Jun NH2-terminal Kinase Activation in Interferon-alpha-induced Apoptosis Through Upregulation of Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) in Daudi B Lymphoma Cells. Exp Cell Res. 2005 Oct 15;310(1):10-21. PubMed PMID: 16099454.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Requirement of c-Jun NH2-terminal kinase activation in interferon-alpha-induced apoptosis through upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in Daudi B lymphoma cells. AU - Yanase,Noriko, AU - Hata,Kikumi, AU - Shimo,Kuniaki, AU - Hayashida,Miho, AU - Evers,B Mark, AU - Mizuguchi,Junichiro, PY - 2005/02/16/received PY - 2005/06/23/revised PY - 2005/06/29/accepted PY - 2005/8/16/pubmed PY - 2005/11/15/medline PY - 2005/8/16/entrez SP - 10 EP - 21 JF - Experimental cell research JO - Exp Cell Res VL - 310 IS - 1 N2 - Interferon alpha (IFN-alpha) inhibits growth, at least in part, through induction of apoptosis. However, the molecular mechanisms underlying IFN-alpha-induced apoptosis are not completely understood. In the present study, we found that IFN-alpha induced a sustained activation of c-Jun N-terminal kinase 1 (JNK1), but not extracellular kinases (ERKs), in Daudi B lymphoma cells, as assessed by Western blotting using phospho-specific antibodies. Several lines of evidence support the notion that the IFN-alpha-induced activation of JNK is responsible for IFN-alpha-induced apoptosis, at least in part, through upregulation of TNF-related apoptosis-inducing ligand (TRAIL). First, pretreatment of Daudi cells with a JNK inhibitor reduced IFN-alpha-induced upregulation of TRAIL and loss of mitochondrial membrane potential (DeltaPsim) and annexin-positive cells, which was assessed by flow cytometry. Second, a dominant-negative form of JNK1 (dnJNK1) also reduced these apoptotic events, while a constitutively active form of JNK1, MKK7-JNK1beta, enhanced them. Finally, treatment with IFN-alpha enhanced the promoter activity of the TRAIL gene, which was partially abrogated by either JNK inhibitor or dnJNK1, while it was moderately enhanced by MKK7-JNK1beta. These findings are useful for understanding molecular mechanisms of IFN-alpha-induced apoptosis and also for development of treatment modalities of some tumors with IFN-alpha. SN - 0014-4827 UR - https://www.unboundmedicine.com/medline/citation/16099454/Requirement_of_c_Jun_NH2_terminal_kinase_activation_in_interferon_alpha_induced_apoptosis_through_upregulation_of_tumor_necrosis_factor_related_apoptosis_inducing_ligand__TRAIL__in_Daudi_B_lymphoma_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(05)00305-8 DB - PRIME DP - Unbound Medicine ER -