Here, we show that JNK1 and JNK3 have different roles in TNF-alpha- or etoposide-induced apoptosis in HeLa cells. Dominant negative JNK1 inhibited TNF-alpha- or etoposide-induced apoptosis, while dominant negative JNK3 promoted TNF-alpha- or etoposide-induced apoptosis. During TNF-alpha-induced apoptosis, JNK1 was activated in a biphasic manner, exhibiting both transient and sustained activity, whereas JNK3 was activated early and in a transient manner. The role of JNK3 activation was an anti-apoptotic effect, while the role of JNK1 activation was a pro-apoptotic effect. These results suggest that the anti-apoptotic mechanism of JNK3 in TNF-alpha-induced apoptosis originates before the apoptotic machinery is triggered.
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http://dx.doi.org/10.1007/s10059-009-0160-6 | DOI Listing |
J Cancer Res Clin Oncol
December 2023
School of Basic Medicine, Hainan Medical University, Haikou, 571199, China.
Purpose: Mitogen-activated protein kinases (MAPK), specifically the c-Jun N-terminal kinase (JNK)-MAPK subfamily, play a crucial role in the development of various cancers, including hepatocellular carcinoma (HCC). However, the specific roles of JNK1/2 and their upstream regulators, MKK4/7, in HCC carcinogenesis remain unclear.
Methods: In this study, we performed differential expression analysis of JNK-MAPK components at both the transcriptome and protein levels using TCGA and HPA databases.
FASEB J
January 2021
Guizhou Provincial Key Laboratory of Pathogenesis and Drug Research on Common Chronic Diseases, Guizhou Medical University, Guiyang, China.
Etoposide-induced 2.4 (EI24) exerts tumor suppressor activity through participating in cell apoptosis, autophagy, and inflammation. However, its role in renal diseases has not been elucidated.
View Article and Find Full Text PDFMol Cancer
March 2015
Cell Signaling and Apoptosis Group, Fundacio Institut de Recerca de l'Hospital Universitari de la Vall d'Hebron, Edifici Collserola, Passeig Vall d'Hebron 119-129, 08035, Barcelona, Spain.
Background: Patients with high-risk neuroblastoma (NBL) tumors have a high mortality rate. Consequently, there is an urgent need for the development of new treatments for this condition. Targeting death receptor signaling has been proposed as an alternative to standard chemo- and radio-therapies in various tumors.
View Article and Find Full Text PDFCell Death Dis
February 2015
Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School (UMMS), Worcester, MA 01655, USA.
Apoptosis is a key mechanism for metazoans to eliminate unwanted cells. Resistance to apoptosis is a hallmark of many cancer cells and a major roadblock to traditional chemotherapy. Recent evidence indicates that inhibition of caspase-dependent apoptosis sensitizes many cancer cells to a form of non-apoptotic cell death termed necroptosis.
View Article and Find Full Text PDFActa Pol Pharm
June 2013
Department of Biotechnology and Genetic Engineering, Medical University of Silesia in Katowice, Narcyzów 1, 41-200 Sosnowiec, Poland.
BCL-2 and C-RAF genes are overexpressed in most types of cancers. Although these genes are mediators in different molecular pathways their main characteristic is the antiapoptotic activity, thus cells that overexpress either BCL-2 or C-RAF lose their ability to undergo apoptotic death being resistant to chemotherapeutic agents and/or physiologic mediators of cell death (e.g.
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