Distinct roles for JNK1 and JNK3 during TNF-alpha- or etoposide-induced apoptosis in HeLa cells.

Mol Cells

Division of Pharmaceutical Biosciences, College of Pharmacy and the Research Institute for Pharmaceutical Sciences, Seoul National University, Seoul, 151-742, Korea.

Published: December 2009

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.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10059-009-0160-6DOI Listing

Publication Analysis

Top Keywords

tnf-alpha- etoposide-induced
16
etoposide-induced apoptosis
16
jnk1 jnk3
8
apoptosis hela
8
hela cells
8
dominant negative
8
tnf-alpha-induced apoptosis
8
jnk3
6
apoptosis
6
jnk1
5

Similar Publications

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.

View Article and Find Full Text PDF

EI24 alleviates renal interstitial fibrosis through inhibition of epithelial-mesenchymal transition and fibroblast activation.

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 PDF

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 PDF

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 PDF

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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!