2nd Edition of International Obesity and Metabolism Conference 2026

Abstract

Cancer cells often rewire their metabolic processes to adapt to environments that are low in nutrients and oxygen, which promotes both proliferation and metastasis. Lipid metabolism is particularly important because lipids serve as both energy sources and signaling molecules within cell membranes. Our research has highlighted the crucial role of hypoxia-inducible factor-1 (HIF-1) in lipid metabolic reprogramming in cancer cells. HIF-1 acts as a master transcription factor that drives tumor growth and metastasis by activating genes associated with proliferation, survival, angiogenesis, invasion, and metabolism. Additionally, HIF-1 contributes to cancer progression by modifying lipid accumulation, beta-oxidation, and lipolysis. To explore the potential role of HIF-1 in the interaction between lipid metabolism and cancer progression, we discovered that the lipid/HIF-1/chemokine axis promotes tumor proliferation and metastasis in a xenograft mouse model. We also found that lipid-enhanced HIF-1 stimulates the three-dimensional (3D) growth of cancer cells. Utilizing an in vitro model that mimics the tumor microenvironment (TME), we provided new mechanistic insights into how fatty acids released by adipocyte-derived stem cells (ADSCs) act as oncometabolites for cancer cells. Furthermore, our research revealed that cancer cells instruct ADSCs to absorb fatty acids. The chemokines released by cancer cells enhance the expression of lipolysis-related genes in ADSCs via paracrine signaling. In summary, it appears that cancer cells can control adjacent fat tissues through chemokines to extract free fatty acids (FFAs), which they subsequently use for proliferation and migration. Therefore, targeting lipid metabolic alterations mediated by HIF-1 suggests a significant therapeutic potential for cancer treatment.