Abnormal energy metabolism, as one of the important hallmarks of cancer, was induced by multiple carcinogenic factors and tumor-specific microenvironments. It comprises aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis. Considering that metabolic reprogramming provides various nutrients for tumor survival and development, it has been considered a potential target for cancer therapy. Cannabinoids have been shown to exhibit a variety of anticancer activities by unclear mechanisms. This paper first reviews the recent progress of related signaling pathways (reactive oxygen species (ROS), AMP-activated protein kinase (AMPK), mitogen-activated protein kinases (MAPK), phosphoinositide 3-kinase (PI3K), hypoxia-inducible factor-1alpha (HIF-1α), and p53) mediating the reprogramming of cancer metabolism (including glucose metabolism, lipid metabolism, and amino acid metabolism). Then we comprehensively explore the latest discoveries and possible mechanisms of the anticancer effects of cannabinoids through the regulation of the above-mentioned related signaling pathways, to provide new targets and insights for cancer prevention and treatment.
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http://dx.doi.org/10.1016/j.biopha.2022.113993 | DOI Listing |
Genet Epidemiol
January 2025
Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, Massachusetts, USA.
Large-scale gene-environment interaction (GxE) discovery efforts often involve analytical compromises for the sake of data harmonization and statistical power. Refinement of exposures, covariates, outcomes, and population subsets may be helpful to establish often-elusive replication and evaluate potential clinical utility. Here, we used additional datasets, an expanded set of statistical models, and interrogation of lipoprotein metabolism via nuclear magnetic resonance (NMR)-based lipoprotein subfractions to refine a previously discovered GxE modifying the relationship between physical activity (PA) and HDL-cholesterol (HDL-C).
View Article and Find Full Text PDFFree Radic Res
January 2025
Radiation Biology & Health Sciences Division, Bio-science Group, Bhabha Atomic Research Centre, Trombay, Mumbai-400085, India.
Free radicals have been implicated in the pathogenesis of cancer along with cardiovascular, neurodegenerative, pulmonary and inflammatory disorders. Further, the relationship between oxidative stress and disease is distinctively established. Clinical trials using anti-oxidants for the prevention of disease progression have indicated some beneficial effects.
View Article and Find Full Text PDFPer Med
January 2025
Department of Clinical Pharmacy, Zhejiang Provincial Key Laboratory for Drug Evaluation and Clinical Research, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Efforts have been made to leverage technology to accurately identify tumor characteristics and predict how each cancer patient may respond to medications. This involves collecting data from various sources such as genomic data, histological information, functional drug profiling, and drug metabolism using techniques like polymerase chain reaction, sanger sequencing, next-generation sequencing, fluorescence in situ hybridization, immunohistochemistry staining, patient-derived tumor xenograft models, patient-derived organoid models, and therapeutic drug monitoring. The utilization of diverse detection technologies in clinical practice has made "individualized treatment" possible, but the desired level of accuracy has not been fully attained yet.
View Article and Find Full Text PDFNMR Biomed
February 2025
Department of Biomedical Engineering, Yale University, New Haven, Connecticut, USA.
Cellular metabolism is inextricably linked to transmembrane levels of proton (H), sodium (Na), and potassium (K) ions. Although reduced sodium-potassium pump (Na-K ATPase) activity in tumors directly disturbs transmembrane Na and K levels, this dysfunction is a result of upregulated aerobic glycolysis generating excessive cytosolic H (and lactate) which are extruded to acidify the interstitial space. These oncogene-directed metabolic changes, affecting intracellular Na and H, can be further exacerbated by upregulation of ion exchangers/transporters.
View Article and Find Full Text PDFInt J Surg
January 2025
Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
The immune response is modulated by a diverse array of signals within the tissue microenvironment, encompassing biochemical factors, mechanical forces, and pressures from adjacent tissues. Furthermore, the extracellular matrix and its constituents significantly influence the function of immune cells. In the case of carcinogenesis, changes in the biophysical properties of tissues can impact the mechanical signals received by immune cells, and these signals can be translated into biochemical signals through mechano-transduction pathways.
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