Related Experiment Video
Updated: Jan 2, 2026
Generation of CAR T Cells for Adoptive Therapy in the Context of Glioblastoma Standard of Care
Published on: February 16, 2015
DR5 related autophagy can promote apoptosis in gliomas after irradiation
Peng Zhang1, Hailong Wang1, Yu Chen1
1School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Abstract:
As a cancer treatment strategy, irradiation therapy is widely used that can cause DNA breakage and increase free radicals, which leads to different types of cell death. Among them, apoptosis and autophagy are the most important and the most studied cell death processes. Although the exploration of the relationship between apoptosis and autophagy has been a major area of focus, still the molecular mechanisms of autophagy on apoptosis remain unclear. Here, we have revealed that apoptosis was enhanced by the death receptor 5 (DR5) pathway, and the effect of autophagy on apoptosis was promoted by DR5 interacting with LC3B as well as Caspase8 in gliomas after irradiation. Interestingly, we observed that the addition of four different autophagy inducers, rapamycin (RAP), CCI779, ABT737 and temozolomide (TMZ), induced the differences of DR5 expression and cell apoptosis after irradiation. Unlike RAP and CCI779, ABT737 and TMZ were able to increase DR5 expression and further induce cell death. Therefore, we have concluded that DR5 plays a novel and indispensable role in promoting cell apoptosis under irradiation and suggest a potential therapeutic approach for glioblastoma treatment.
Insights
Irradiation therapy enhances cancer cell death via the death receptor 5 (DR5) pathway. DR5 interacts with autophagy proteins and Caspase8, promoting apoptosis in gliomas and suggesting a new glioblastoma treatment strategy.
Area of Science:
- Oncology
- Cell Biology
- Cancer Therapeutics
Background:
- Irradiation therapy is a common cancer treatment causing DNA damage and cell death, primarily apoptosis and autophagy.
- The interplay between apoptosis and autophagy in response to irradiation remains incompletely understood at the molecular level.
Purpose of the Study:
- To elucidate the molecular mechanisms by which autophagy influences apoptosis in gliomas following irradiation.
- To investigate the role of death receptor 5 (DR5) in mediating the effects of autophagy on irradiation-induced apoptosis.
Main Methods:
- Investigated the interaction between DR5, LC3B, and Caspase8 in glioma cells after irradiation.
- Utilized four autophagy inducers (rapamycin, CCI779, ABT737, temozolomide) to assess their effects on DR5 expression and apoptosis.
Main Results:
- Apoptosis was enhanced by the DR5 pathway, with DR5 interacting with LC3B and Caspase8 to promote autophagy's effect on apoptosis in irradiated gliomas.
- ABT737 and temozolomide increased DR5 expression and cell death, unlike rapamycin and CCI779.
Conclusions:
- DR5 plays a critical role in promoting irradiation-induced apoptosis.
- DR5 targeting represents a potential therapeutic strategy for glioblastoma treatment.
Related Concept Videos
01:18Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
01:30Apoptosis