FASN (Fatty acid synthase)

In both in vitro and in vivo experiments, Jionoside B1 significantly suppressed lipid synthesis and attenuated tumor growth. This study systematically elucidates the mechanism by which low-dose TNF-α regulates lipid metabolism and promotes GBM malignant progression via the TRAF2-FASN axis, providing not only new insights into the "double-edged sword" role of TNF-α in the tumor microenvironment but also a potential novel therapeutic strategy for targeting this pathway in GBM treatment.

Targeting FASN as a modulator of 5-FU resistance, via pharmacological inhibitor and phototoxic peptide conjugate, resensitised cells to 5-FU in acquired organoid models of resistance. PDOs are valuable tools for modelling drug resistance and offer opportunities to discover novel therapeutic approaches to circumvent the emergence of drug resistance.

Additionally, it evaluates emerging therapeutic strategies targeting the metabolic-immune axis, such as inhibitors of HK2 or GLS1 combined with anti-PD-1/PD-L1 agents, which aim to reverse immunosuppression and improve clinical outcomes. By synthesizing recent advances, this work provides a theoretical framework for precision oncology interventions, highlighting the potential of metabolic immunotherapies and future directions integrating AI and multi-omics data to overcome resistance in lung cancer.

This paper systematically reviews the mechanisms underlying therapy-induced metabolic reprogramming in BRAF-mutant melanoma and explores potential combinatorial strategies that target these metabolic vulnerabilities alongside established melanoma therapies. Key metabolic targets with promising therapeutic potential identified include lysine-specific demethylase 1, oxidative phosphorylation components, phosphoglycerate dehydrogenase, indoleamine 2,3-dioxygenase 1 and lipid metabolism enzymes such as fatty acid synthase and 3-hydroxy-3-methylglutaryl-coenzyme a reductase.

Its mechanism of action involves the suppression of lipid synthesis and the prevention of hepatocyte apoptosis, achieved by modulating key anti-inflammatory and antioxidant signaling pathways. Flavonoids (such as apigenin and quercetin) are identified as the key active ingredients in DXR responsible for activating Keap1/Nrf2 and PI3K/AKT signaling pathways.

GRE shows promising potential as a natural treatment option for NAFLD.

Therefore, aberrant CREs acts as "metabolic switches" that sense and respond to various metabolic conditions to sustain HCC growth. Consequently, targeted intervention against oncogenic CREs, such as super-enhancers or their co-activators, to disrupt CRE-mediated metabolic vulnerabilities, has emerged as a highly promising new paradigm for precision therapy in HCC.

Co-expression of these key metabolic enzymes remains a promising candidate as prognostic markers and therapeutic targets. Concurrent targeting of these metabolic pathways may offer novel therapeutic opportunities for patients with advanced-stage gastric cancer.

Notably, clinically relevant SMAD4 mutants (R361C and R361H) exhibit enhanced palmitoylation, underscoring the pathological relevance of this mechanism for tumorigenesis. Collectively, these findings unveil a metabolic-transcriptional circuit wherein palmitoylation bridges lipid metabolism with SMAD4-driven oncogenesis, and posit SMAD4 palmitoylation as a therapeutic vulnerability in pancreatic cancer.

AKR1C1 activation drived lipid metabolic dysregulation characterized by enhanced fatty acid synthesis, thereby facilitating metabolic adaptation and survival during early LUSC carcinogenesis. Collectively, our findings identified AKR1C1 as an early-response biomarker and a pivotal metabolic node controlling FASN-dependent lipid metabolic reprogramming in LUSC.

In addition, adipo-8-LEVs-cur did not cause any damage to other organs. These results suggest that the adipo-8-LEVs-cur delivery system provides an idea for obesity treatment targeting adipocytes, which is of practical significance for anti-obesity research.

The ESM1-ANGPTL4-FASN-trioleate axis orchestrates metabolic reprogramming and endothelial activation, representing a promising therapeutic target. Future studies should explore combination therapies targeting this axis and overcoming bevacizumab resistance in HCC.