Cancerwise

Metabolism is the process by which the cells in your body use nutrients from the food you eat to get the energy you need. 

When we talk about cancer metabolism, we’re talking about the process in which cancer cells make the energy they need to grow and spread. For nearly a century, cancer researchers have been working to develop a deeper understanding of cancer metabolism in hopes that it could lead to better treatment and prevention techniques. 

In 2025, several MD Anderson research teams helped push cancer metabolism from a biochemical curiosity to a central framework for understanding, and potentially treating, metastatic disease. Two recent publications illustrate how metabolic rewiring shapes tumor aggression, how organs function and what therapeutic opportunities may lie ahead.

1. Sugary Drinks and Colorectal Cancer Metastasis — A Metabolic Mechanism With Real-World Impact (Nature Metabolism, Jihye Yun Lab)

What do sugar-sweetened beverages do to cancer cells? A group led by Jihye Yun, Ph.D., assistant professor, Genetics, uncovered a surprisingly potent metabolic driver of metastasis, or how cancer spreads.

Their study, published in Nature Metabolism, demonstrates that a glucose–fructose mixture, mimicking common sugary drinks, reprograms colorectal cancer metabolism as sugar breaks down. This shift increases the ratio of energy production to energy consumption at the cellular level and funnels carbon into the cholesterol biosynthesis pathway, which promotes cell migration and the start of metastasis.  

Highlights of this work:

• It provides a mechanistic explanation for how dietary sugar can enhance the potential for metastasis.
• It shows that two parts of how cells process energy — the breakdown of sugar, and the pathway the body uses to create cholesterol, known as cholesterol biosynthesis — can be targeted to change cell metabolism.
• It raises the intriguing possibility that statins, common cholesterol-lowering prescription drugs, may dampen this metastasis-promoting circuit.

Takeaway: Diet is not just about your lifestyle. It is a metabolic input that can modulate metastasis through rewired biochemical pathways. 

2. Fatty Acid Metabolism as a Driver of Bone Metastasis — ACBP as a Key Regulator (Science Translational Medicine, Li Ma Lab)

The second highlight comes from Li Ma, Ph.D., professor, Experimental Radiation Oncology, who uncovered a metabolic determinant of bone metastasis that goes far beyond glycolysis, the process of converting sugar to energy.

Their translational medicine study shows that ACBP, a specific protein that binds to acyl-CoA, a form of fatty acid, supports the spread of cancer to bone by tuning fatty-acid oxidation (FAO) and protecting tumor cells from ferroptosis, an iron-dependent form of cell death. Tumor cells that rely on this ACBP-FAO axis gain a survival advantage in the lipid-rich, high-stress bone microenvironment. 

Highlights of this work:

• It places lipid metabolism, the process of breaking down fats for energy, at the center of metastatic biology. 
• It suggests fatty-acid oxidation inhibitors or ferroptosis-sensitizing strategies as therapeutic avenues for bone metastatic disease. 
• It strengthens a broader theme: metastatic cells survive by re-wiring metabolic stress responses. 

Takeaway: Bone metastasis is not just about niche interactions; it is powered by a lipid-metabolic adaptation that can be targeted.

Across these studies, a unifying concept emerges: Metastasis is a metabolic state. Tumor cells that spread must reshape their nutrient use, redox balance, and stress-survival pathways. Those adaptations expose new intervention points.

Whether it is sugary beverages driving pro-metastatic fluctuation via SORD, or lipid metabolism sustaining bone-tropic cancer cells through ACBP, these papers highlight how understanding cancer metabolism is reshaping both prevention and therapy.

Eyal Gottlieb, Ph.D., is vice president of Research at MD Anderson.

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