Cancer Cell Metabolism
Cancer Cell Metabolism - Related Videos
10:19
An Introduction to Cell Metabolism
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2023
In cells, critical molecules are either built by joining together individual units like amino acids or nucleotides, or broken down into smaller components. Respectively, the reactions responsible for this are referred to as anabolic and catabolic. These reactions require or produce energy typically in the form of a “high-energy” molecule called ATP. Together, these processes make up “Cell Metabolism,” and are hallmarks of healthy, living cells.JoVE’s introduction to cell metabolism briefly...
10:51
Preparation and Metabolic Assay of 3-dimensional Spheroid Co-cultures of Pancreatic Cancer Cells and Fibroblasts
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Cited by 31 •
2017
Here, a method is described for the preparation of 3-dimensional (3D) spheroid co-culture of pancreatic cancer cells and fibroblasts, followed by measurement of metabolic functions using an extracellular flux analyzer.
07:29
Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
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Cited by 27 •
2015
Pancreatic cancer stem cells (CSCs) can be expanded in vitro using the anchorage-independent sphere culture technique, which represents a powerful tool to study CSC biology and can serve as the first step to develop novel CSC-targeting therapies. Here the methodology for expanding, analyzing and targeting of pancreatic CSCs is provided.
04:05
Methyl Thiazolyl Tetrazolium or MTT Assay: A Colorimetric Assay to Measure Drug Resistance via Determination of Metabolic Activity in Cancer Cells
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2023
This video describes the colorimetric assay, methyl thiazole tetrazolium (MTT) assay, to measure drug-induced cytotoxicity in cancer cells and determine their metabolic activity. This assay is based on the metabolic conversion of tetrazolium salts into colored products, reflecting the mitochondrial activity of cells.
10:36
Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
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Cited by 5 •
2016
Integration of data from genome-wide sequencing experiments and metabolomics experiments is a challenge. In this paper we report, for the first time, generation, analysis and integration of transcriptome, cistrome and metabolome data from breast cancer cells treated with estradiol.
FAQs
Oncogenic signaling and hypoxia can shift how malignant cells allocate nutrients. Under these influences, cells often increase glucose uptake and favor aerobic glycolysis, even while oxygen-related metabolic conditions are changing. This reprogramming can support rapid growth by supplying usable energy and redirecting metabolic carbon toward the molecular materials required for proliferation.
Redirecting carbon into nucleotide, lipid, and amino acid synthesis supplies the molecular building blocks needed for continued cell production. This means that altered nutrient use supports more than immediate energy generation: it can sustain the biosynthetic demands of proliferation. Tracking these routes therefore helps explain how metabolic reprogramming contributes to malignant growth.
Glutamine metabolism and mitochondrial oxidative phosphorylation give tumor cells additional metabolic routes when their demands change. Cancer cell metabolism therefore cannot be considered only through glucose use or aerobic glycolysis; it also includes alternative nutrient processing and mitochondrial energy production. Considering these routes together helps researchers evaluate how cells sustain growth under differing metabolic conditions.
Metabolic adaptations connect molecular events inside malignant cells with broader tumor behavior. Oncogenic signaling and local conditions such as hypoxia can alter nutrient use, while the resulting metabolic state relates to progression and treatment response. Examining these links places pathway changes in biological context rather than treating metabolism as an isolated source of cellular energy.
Studying altered nutrient use can help identify metabolic vulnerabilities, biomarkers, and therapeutic strategies. These findings can show which metabolic features are relevant to cancer growth or treatment response and can guide efforts to disrupt tumor expansion. The broader objective is to target cancer-associated metabolism while limiting effects on normal tissues.
A therapy targeting tumor metabolism must be evaluated not only for its ability to disrupt cancer growth but also for whether it limits effects on normal tissues. This selectivity is an important challenge in treatment design. Understanding pathway adaptations can help researchers connect a metabolic vulnerability with strategies that are more appropriate for the surrounding biological context.