Related Experiment Video

Updated: Mar 29, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

17.4K

Endocrine control of one-carbon metabolism in cachexia

Yongrui Hai1, Xuejing Duan1, Gaofei Wei1

  • 1Laboratory of Cellular Metabolism and Precision Therapeutics, School of Life Sciences and Technology, Northwestern Polytechnical University, Xi'an 710129, China; Research & Development Institute of Northwestern Polytechnical University, Shenzhen 518057, China.

Trends in Endocrinology and Metabolism: TEM
|March 27, 2026
PubMed

Insights

Cancer cachexia treatments are limited because its causes are not fully understood. A new study reveals one-carbon metabolism links tumor signals to muscle wasting and energy loss, identifying methyl-donor pathways as potential therapeutic targets.

Area of Science:

  • Endocrinology
  • Metabolic pathways
  • Oncology

Background:

  • Cancer cachexia is a complex metabolic syndrome characterized by muscle wasting and systemic inflammation.
  • Current therapeutic strategies for cancer cachexia are limited due to an incomplete understanding of its underlying mechanisms.

Purpose of the Study:

  • To investigate the role of one-carbon metabolism in the development of cancer cachexia.
  • To identify novel therapeutic targets for cancer cachexia by elucidating its upstream drivers.

Main Methods:

  • The study by Morigny et al. explored the endocrine-metabolic program linking tumor signals to skeletal muscle hypermetabolism.
  • Analysis focused on conserved pathways, particularly methyl-donor pathways within one-carbon metabolism.

Main Results:

  • One-carbon metabolism was identified as a key conserved endocrine-metabolic program in cancer cachexia.
  • This metabolic program links tumor-derived signals to skeletal muscle hypermetabolism and systemic energy imbalance.

Conclusions:

  • One-carbon metabolism represents a critical link between cancer and systemic metabolic dysfunction.
  • Methyl-donor pathways within one-carbon metabolism are highlighted as actionable therapeutic targets for treating cancer cachexia.
Keywords:
IL-6cancer cachexiaglucose hypermetabolismmuscle atrophyone-carbon metabolism

More Related Videos

Evaluation of Amino Acid Consumption in Cultured Bone Cells and Isolated Bone Shafts06:32

Evaluation of Amino Acid Consumption in Cultured Bone Cells and Isolated Bone Shafts

Published on: April 13, 2022

2.2K
Quantification of Coenzyme A in Cells and Tissues08:51

Quantification of Coenzyme A in Cells and Tissues

Published on: September 27, 2019

9.1K

Related Concept Videos

Regulation of Metabolism01:19

Regulation of Metabolism

Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
12.3K
Overview of Protein Metabolism01:21

Overview of Protein Metabolism

Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
4.6K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.5K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.4K
Amino Acid Catabolism01:18

Amino Acid Catabolism

Microorganisms rely on proteins as an essential carbon and energy source, particularly in environments with limited polysaccharides or lipids. However, proteins are too large to cross the plasma membrane unaided, necessitating enzymatic degradation. Microbes secrete extracellular proteases and peptidases that hydrolyze proteins into peptides, which can then be transported across the membrane. Once inside the cell, intracellular proteases degrade these peptides into free amino acids, which...
1.6K
Carbohydrate Catabolism01:30

Carbohydrate Catabolism

Carbohydrate catabolism is a fundamental process in cellular metabolism that enables energy extraction from glucose through two primary pathways: cellular respiration and fermentation. Both pathways begin with glycolysis, which operates independently of oxygen availability.Glycolysis: A Shared Starting PointGlycolysis is an oxygen-independent process that breaks down glucose into two molecules of pyruvic acid. During this process, a net gain of two ATP molecules and two NADH molecules is...
1.5K