Related Experiment Video
Updated: Feb 7, 2026
12:12
Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
Published on: June 16, 2011
14.0K
Clusterin, a Novel DEC1 Target, Modulates DNA Damage-Mediated Cell Death
Xin Ming1, Chenyi Bao1, Tao Hong1
1MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu Province, China.
Molecular Cancer Research : MCR
|July 14, 2018
Summary
Differentiated embryonic chondrocyte expressed gene 1 (DEC1) targets clusterin (CLU) to suppress DNA damage-induced cell death in cancer. This DEC1-CLU pathway offers a potential therapeutic target for breast cancer treatment.
Area of Science:
- Molecular biology
- Cancer research
- Cellular signaling
Background:
- Differentiated embryonic chondrocyte expressed gene 1 (DEC1) is a transcription factor involved in various cellular processes, including apoptosis and tumor cell transitions.
- Secretory clusterin (sCLU) is a protective protein that defends against genotoxic stress.
Purpose of the Study:
- To identify novel target genes of DEC1.
- To elucidate the role of the DEC1-CLU axis in DNA damage response and breast cancer cell survival.
Main Methods:
- Chromatin immunoprecipitation assays
- Luciferase reporter assays
- Gene knockdown experiments in MCF7 breast cancer cells
Main Results:
- Clusterin (CLU) was identified as a novel target gene of DEC1.
- DEC1 directly binds to and activates the CLU promoter, increasing sCLU expression.
- DEC1 and sCLU overexpression inhibit DNA damage-induced apoptosis in breast cancer cells.
Conclusions:
- DEC1 functions as a prosurvival factor by upregulating sCLU, thereby reducing apoptosis in response to DNA damage.
- The DEC1-CLU pathway modulates sensitivity to DNA damage, presenting a potential therapeutic strategy for breast cancer.
Related Concept Videos
02:36DNA Damage Can Stall the Cell Cycle
3.2K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.2K
02:36DNA Damage can Stall the Cell Cycle
10.1K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
10.1K
01:18Autophagic Cell Death
4.6K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.6K
01:30Overview of Cell Death
10.2K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
10.2K
02:25Overview of DNA Repair
33.8K
In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Chemically...
33.8K
01:20Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein
922
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
922