A5110601473- Mitochondrial Function and Pathology
- Sirtuins and Resveratrol in Medicine
- Bone health and treatments
- Cancer, Hypoxia, and Metabolism
- Cancer, Lipids, and Metabolism
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- Prostate Cancer Treatment and Research
- Pancreatic function and diabetes
- Click Chemistry and Applications
- Cancer Genomics and Diagnostics
- Cancer survivorship and care
- Adenosine and Purinergic Signaling
- Optimism, Hope, and Well-being
- Cancer-related Molecular Pathways
- Radiopharmaceutical Chemistry and Applications
- Health and Wellbeing Research
Roswell Park Comprehensive Cancer Center
2019-2022
Baylor College of Medicine
2019
Metabolic dysregulation is a known hallmark of cancer progression, yet the oncogenic signals that promote metabolic adaptations to drive metastatic remain unclear. Here, we show transcriptional repression mitochondrial deacetylase sirtuin 3 (
<div>Abstract<p>Metabolic dysregulation is a known hallmark of cancer progression, yet the oncogenic signals that promote metabolic adaptations to drive metastatic remain unclear. Here, we show transcriptional repression mitochondrial deacetylase sirtuin 3 (<i>SIRT3</i>) by androgen receptor (AR) and its coregulator steroid coactivator-2 (SRC-2) enhances aconitase (ACO2) activity favor aggressive prostate cancer. ACO2 promoted citrate synthesis facilitate <i>de...
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<div>Abstract<p>Metabolic dysregulation is a known hallmark of cancer progression, yet the oncogenic signals that promote metabolic adaptations to drive metastatic remain unclear. Here, we show transcriptional repression mitochondrial deacetylase sirtuin 3 (<i>SIRT3</i>) by androgen receptor (AR) and its coregulator steroid coactivator-2 (SRC-2) enhances aconitase (ACO2) activity favor aggressive prostate cancer. ACO2 promoted citrate synthesis facilitate <i>de...
Abstract Background: Metabolic rewiring is one of the central hallmarks cancer progression and survival to support anabolic energetic demands. Tumor cells constantly alter their metabolic state in response oncogenic stimuli, nutrient availability, interaction with immune however precise regulation that precedes alteration poorly understood. Here we report a direct glycolytic enzyme PFKFB4 transcriptional coregulator SRC-3. functions as critical regulator Warburg effect our study reveals upon...
Abstract Prostate cancer (PCa) is the most common and second leading cause of death among men in America. Aggressive prostate tumors that rapidly metastasize to other organs such as bones account for high morbidity mortality. Metastatic PCa resistant androgen depletion therapy, increased expression receptor (AR) coregulator Steroid Receptor Coregulator-2 (SRC-2) remains a major underlying driver lethal progression. Increased SRC-2 positively correlates with recurrence poor disease outcome....
Abstract Background: Accumulation of extracellular adenosine regulates tumor progression. Extracellular binds to receptors, which mediates signaling induce angiogenesis and cell proliferation, as well functioning an immunosuppressive agent in the microenvironment (TME). CD73 CD39 are two surface enzymes that catalyze synthesis from AMP, ADP ATP TME. However, underlying mechanisms regulate TME ER-positive breast cancer remains unknown. Methods: In order investigate transcriptional regulation...
Cancer cells encounter a hostile tumor microenvironment (TME) and their ability to successfully adapt by mitigating stress responses determine metastatic competence. However, the underlying mechanisms that reprogram intrinsic adaptations leading an invasive cancer phenotype remains elusive. Here, we demonstrate metabolic enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-4 (PFKFB4) is induced in hypoxic tumors acquiring plasticity phenotype. In mouse models of breast cancer, genetic...
Abstract Cancer cells have acquired the ability to sense and adapt varying conditions of nutrient sources in tumor microenvironment. Mitochondria lay at core cellular metabolism, whereas nucleus integrates environmental signals activate gene transcription that alter cell function fate. However, it remains largely unexplored how mitochondrial metabolic enzymes nuclear transcriptional machineries communicate drive regulation response stress. Biochemical screening identified a TCA cycle enzyme...