AI Article Synopsis
- Regulation of metabolic pathways, particularly through TIGAR, is crucial for cell growth and survival, influencing processes like antioxidant production and nucleotide synthesis.
- Though TIGAR is not needed for normal mouse development, it is essential for intestinal regeneration, with defects mitigated by ROS scavengers and nucleosides.
- In a mouse model, TIGAR deficiency led to reduced tumor burden and improved survival, while increased TIGAR levels in human colon tumors indicate its role in cancer progression, highlighting it as a potential therapeutic target for conditions like ulcerative colitis and intestinal cancer.
Article Abstract
Regulation of metabolic pathways plays an important role in controlling cell growth, proliferation, and survival. TIGAR acts as a fructose-2,6-bisphosphatase, potentially promoting the pentose phosphate pathway to produce NADPH for antioxidant function and ribose-5-phosphate for nucleotide synthesis. The functions of TIGAR were dispensable for normal growth and development in mice but played a key role in allowing intestinal regeneration in vivo and in ex vivo cultures, where growth defects due to lack of TIGAR were rescued by ROS scavengers and nucleosides. In a mouse intestinal adenoma model, TIGAR deficiency decreased tumor burden and increased survival, while elevated expression of TIGAR in human colon tumors suggested that deregulated TIGAR supports cancer progression. Our study demonstrates the importance of TIGAR in regulating metabolism for regeneration and cancer development and identifies TIGAR as a potential therapeutic target in diseases such as ulcerative colitis and intestinal cancer.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682186 | PMC |
| http://dx.doi.org/10.1016/j.devcel.2013.05.001 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
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!