# Metabolic reprogramming in bone metastasis of human cancers

## TL;DR

Cancer cells change their metabolism to survive and grow in bone metastasis, and targeting these changes could lead to new treatments.

## Contribution

The paper highlights how metabolic reprogramming enables tumor survival in the bone metastatic microenvironment and suggests targeting these metabolic adaptations as a therapeutic strategy.

## Key findings

- Tumor cells alter glycolysis, oxidative phosphorylation, lipid, and amino acid metabolism to adapt to bone metastasis.
- The bone metastatic environment is characterized by hypoxia and acidity, requiring metabolic adaptations for tumor survival.
- Targeting metabolic dependencies in tumor-bone stroma interactions could disrupt metastatic progression.

## Abstract

Bone metastasis represents a complex complication of advanced human malignancies. Metabolic reprogramming plays a critical role in bone metastasis. Tumor cells hijack and alter local metabolic pathways to fuel their energetic and biosynthetic demands for proliferation and survival within the bone metastatic microenvironment. This includes adaptations in glycolysis, oxidative phosphorylation, lipid metabolism and amino acid metabolism. Furthermore, this bone metastatic microenvironment exhibits distinct metabolic features, such as hypoxia and acidity. To survive in this hostile microenvironment, tumor cells that metastasize to bone have to undergo metabolic reprogramming. Collectively, understanding the intricate link between metabolic reprogramming and bone metastasis is crucial for developing novel therapeutic strategies. Targeting the specific metabolic addiction and interrupting the nutrient-based crosstalk between tumor cells and the bone stroma offers a promising way to inhibit the vicious cycle and bone metastatic progression.