Fig. 1: Glucose metabolism and lipid metabolism reprogramming in RCC.
From: The pathogenesis and therapeutic implications of metabolic reprogramming in renal cell carcinoma
The balance between gluconeogenesis and glycolysis is intricately regulated during kidney cancer progression. The reciprocal regulatory interaction between FBP1 and EZH2, key components of gluconeogenic pathways, has been identified as a potential therapeutic target for renal cell carcinoma (RCC). In contrast, the glycolysis-associated gene DEPDC1 plays a pivotal role in driving malignant progression and drug resistance in RCC, suggesting that glycolysis inhibitors such as 3BrPA may offer promising targeted therapeutic options for ccRCC. Additionally, PFKFB4 has been shown to mediate resistance to sunitinib by enhancing the pentose phosphate pathway (PPP). Meanwhile, ubiquinone-cytochrome c reductase hinge protein (UQCRH) and circFOXP1 influence RCC progression through their impact on the Warburg effect. RCC progression is significantly influenced by key enzymes involved in the fatty acid metabolic pathway. Malonyl coenzyme A decarboxylase (MLYCD) and E3 ubiquitin ligase TRIM21 suppress tumor progression by inhibiting fatty acid synthesis and promoting fatty acid oxidation. Conversely, the AMPK-GATA3-ECHS1 pathway facilitates fatty acid synthesis and supports cancer cell proliferation. Additionally, hypoxia-inducible factors (HIFs) inhibit fatty acid oxidation by downregulating carnitine palmitoyltransferase 1 (CPT1). Created by Biorender.com. RCC renal cell carcinoma, UQCRH ubiquinone-cytochrome c reductase hinge protein, PPP pentose phosphate pathway, MLYCD malonyl coenzyme A decarboxylase, HIFs hypoxia-inducible factors, CPT1 carnitine palmitoyltransferase 1.
