A5031428360- Cancer, Hypoxia, and Metabolism
- Diet and metabolism studies
- Amino Acid Enzymes and Metabolism
- Mitochondrial Function and Pathology
- Synthesis and biological activity
- Drug Transport and Resistance Mechanisms
- Radiopharmaceutical Chemistry and Applications
- Inflammatory mediators and NSAID effects
- Angiogenesis and VEGF in Cancer
- Nanoplatforms for cancer theranostics
- ATP Synthase and ATPases Research
- Peroxisome Proliferator-Activated Receptors
- Synthesis and Biological Evaluation
- Metabolomics and Mass Spectrometry Studies
- Autophagy in Disease and Therapy
- Ubiquitin and proteasome pathways
- Cannabis and Cannabinoid Research
- Synthesis and Catalytic Reactions
- Pancreatic function and diabetes
- Apelin-related biomedical research
- Cancer-related Molecular Pathways
- Chemical Synthesis and Analysis
- Lanthanide and Transition Metal Complexes
- Bladder and Urothelial Cancer Treatments
- Graphene and Nanomaterials Applications
Janssen (Belgium)
2023
UCLouvain
2008-2018
KU Leuven
2017
VIB-KU Leuven Center for Cancer Biology
2017
Abstract Extracellular tumor acidosis largely results from an exacerbated glycolytic flux in cancer and cancer-associated cells. Conversely, little is known about how cells adapt their metabolism to acidosis. Here, we demonstrate that long-term exposure of acidic pH leads a metabolic reprogramming toward glutamine metabolism. This switch triggered by the need reduce production protons glycolysis further maintained NAD+-dependent increase SIRT1 deacetylase activity ensure intracellular...
Abstract Lactate exchange between glycolytic and oxidative cancer cells is proposed to optimize tumor growth. Blocking lactate uptake through monocarboxylate transporter 1 (MCT1) represents an attractive therapeutic strategy but may stimulate glucose consumption by cells. We report here that inhibition of mitochondrial pyruvate carrier (MPC) activity fulfils the tasks blocking use while preventing metabolism. Using in vitro 13 C-glucose vivo hyperpolarized C-pyruvate, we identify 7ACC2 as a...
High lactate concentration in tumors is associated with bad prognosis. Lactate released by glycolytic cells and recaptured oxidative cancer to feed the tricarboxylic acid (TCA) cycle after conversion into pyruvate. Monocarboxylate transporters (MCT) mediate these fluxes of proton-linked represent attractive targets interrupt shuttle inhibit tumor growth. Here, we investigated properties 7-aminocarboxycoumarins (7ACC) developed selectively interfere lactate-rich microenvironment. The...
Pyrazolic compounds represent a large source of anticancer compounds, based on the choice scaffold structure, nature substituents and sites coordination. Here, we discuss our recent progresses in identifying new active molecules from synthetic library 14 nitrogen compounds. All these exert antiproliferative activity against breast colorectal cancer cell lines with varying IC50 values (the half-maximal inhibitory concentration, which is measure effectiveness compound inhibiting biological or...
The synthesis and structure – activity relationships (SAR) antitumor activities of monopyrazolic bipyrazolic tripodal derivatives are reported here for the first time. ten products were tested against three human cancer cell lines including breast (MDA-MB231), prostate (PC3) colorectal (LoVo) cancers. In series, most them exhibited a moderate with an order 5 > 7 8 in case ≉ Keywords: Antitumor activity, Bipyrazoles, LoVo, MDA-MB231, PC3, Synthesis, Pyrazole derivatives, biologically active...
Abstract Conventional models for preclinical drug screening offer poor predictive value patient response, causing high attrition rates of new agents in the clinic. HUB’s proprietary Patient-Derived Organoid (PDO) Technology enables long-term expansion primary material to generate ‘mini organs a dish’ that can be used as avatars, thus bringing every “patient lab®”. We present world’s first NMIBC PDO biobank comprising 50 from transurethral resection bladder (TURB) biopsies collected at three...
<p>Supplementary Figure S4. HIF acetylation is regulated by acidosis-triggered SIRT1 activity.</p>
<p>Supplementary Figure S5. Acidosis-triggered metabolic shift is reversible in FaDu and HCT-116 tumor cells.</p>
<p>Supplementary Figure S6. Model of metabolic adaptation tumor cells under chronic low pH conditions.</p>
<p>Supplementary Figure S2. Chronic acidosis increases amino-acid uptake.</p>
<p>Supplementary Figure S1. Chronic acidosis causes a metabolic switch from glucose to glutamine utilization in FaDu and HCT-116 tumor cells.</p>