AI Article Synopsis
- PARP10 is a member of the PARP family known for its role in mono-ADP-ribosylation of proteins and has been linked to metabolic processes.
- Silencing PARP10 in cancer cell models led to enhanced mitochondrial oxidative capacity, reduced oxidative stress, and greater expression of antioxidant genes, resulting in decreased cell proliferation.
- Lower expression of PARP10 is associated with improved survival rates in gastric cancer and is influenced by metabolic conditions like fasting, which promotes mitochondrial biogenesis and fatty acid oxidation.
Article Abstract
Poly(ADP-ribose) polymerase (PARP)10 is a PARP family member that performs mono-ADP-ribosylation of target proteins. Recent studies have linked PARP10 to metabolic processes and metabolic regulators that prompted us to assess whether PARP10 influences mitochondrial oxidative metabolism. The depletion of PARP10 by specific shRNAs increased mitochondrial oxidative capacity in cellular models of breast, cervical, colorectal and exocrine pancreas cancer. Upon silencing of PARP10, mitochondrial superoxide production decreased in line with increased expression of antioxidant genes pointing out lower oxidative stress upon PARP10 silencing. Improved mitochondrial oxidative capacity coincided with increased AMPK activation. The silencing of PARP10 in MCF7 and CaCo2 cells decreased the proliferation rate that correlated with increased expression of anti-Warburg enzymes (Foxo1, PGC-1α, IDH2 and fumarase). By analyzing an online database we showed that lower PARP10 expression increases survival in gastric cancer. Furthermore, PARP10 expression decreased upon fasting, a condition that is characterized by increases in mitochondrial biogenesis. Finally, lower PARP10 expression is associated with increased fatty acid oxidation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5749700 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0187789 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
ANAC044 orchestrates mitochondrial stress signaling to trigger iron-induced stem cell death in root meristems.
Proc Natl Acad Sci U S A
January 2025
Ministry of Education Key Laboratory of Environment Remediation and Ecological Health, Zhejiang Provincial Key Laboratory of Agricultural Resources and Environment, College of Environmental and Resource Sciences, Zhejiang University, Hangzhou 310058, China.
While iron (Fe) is essential for life and plays important roles for almost all growth related processes, it can trigger cell death in both animals and plants. However, the underlying mechanisms for Fe-induced cell death in plants remain largely unknown. S-nitrosoglutathione reductase (GSNOR) has previously been reported to regulate nitric oxide homeostasis to prevent Fe-induced cell death within root meristems.
View Article and Find Full Text PDFFirst report of a major management target species, chironomid Paratanytarsus grimmii (Diptera: Chironomidae) larvae, in drinking water treatment plants (DWTPs) in South Korea.
PLoS One
January 2025
Department of Ocean Integrated Science, Chonnam National University, Yeosu, Korea.
Ensuring the supply of safe and high-quality drinking water can be compromised by the presence of chironomid larvae in drinking water treatment plants (DWTPs), which may contaminate municipal water systems through freshwater resources. Chironomids are dominant species known for their resilience to a broad range of extreme aquatic environments. This study aimed to identify the morphological characteristics and obtain genetic information of the chironomid Paratanytarsus grimmii found in the water intake source and freshwater resource of DWTPs in Korea, highlighting the potential possibility of a parthenogenetic chironomid outbreak within DWTP networks.
View Article and Find Full Text PDFNon-canonical hepatic androgen receptor mediates glucagon sensitivity in female mice through the PGC1α/ERRα/mitochondria axis.
Cell Rep
January 2025
Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, Zhejiang, China; Key Laboratory of Growth Regulation and Translational Research of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China; Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou, Zhejiang, China; Research Center for Industries of the Future, Westlake University, Hangzhou, Zhejiang, China. Electronic address:
Glucagon has recently been found to modulate liver fat content, in addition to its role in regulating gluconeogenesis. However, the precise mechanisms by which glucagon signaling synchronizes glucose and lipid metabolism in the liver remain poorly understood. By employing chemical and genetic approaches, we demonstrate that inhibiting the androgen receptor (AR) impairs the ability of glucagon to stimulate gluconeogenesis and lipid catabolism in primary hepatocytes and female mice.
View Article and Find Full Text PDFPrevious short-term disuse dictates muscle gene expression and physiological adaptations to subsequent resistance exercise.
J Physiol
January 2025
Department of Biomedical Sciences, University of Padova, Padova, Italy.
Short-term unloading experienced following injury or hospitalisation induces muscle atrophy and weakness. The effects of exercise following unloading have been scarcely investigated. We investigated the functional and molecular adaptations to a resistance training (RT) programme following short-term unloading.
View Article and Find Full Text PDFMetformin Alleviates Doxorubicin-Induced Cardiotoxicity via Preserving Mitochondrial Dynamics Balance and Calcium Homeostasis.
Appl Biochem Biotechnol
January 2025
Department of Pharmacology, Faculty of Veterinary Medicine, Assiut University, Assiut, 71516, Egypt.
Doxorubicin (DOX) is a commonly used chemotherapeutic medication for treating malignancies, although its cardiotoxicity limits its use. There is growing evidence that alteration of the mitochondrial fission/fusion dynamic processes accompanied by excessive reactive oxygen species (ROS) production and alteration of calcium Ca homeostasis are potential underlying mechanisms of DOX-induced cardiotoxicity (DIC). Metformin (Met) is an AMP-activated protein kinase (AMPK) activator that has antioxidant properties and cardioprotective effects.
View Article and Find Full Text PDFWant 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!