FABP4 (Fatty Acid Binding Protein 4)

In summary, our study demonstrated that long-term exposure to olanzapine increases circulating plasma levels of TNF-α, thus leading to increased expression of FABP4 protein in white adipose tissue and subsequently inhibiting Dhhc7expression, which correspondingly leads to reduced membrane translocation of GLUT4 and consequent insulin resistance. In conclusion, this study elucidated the signalling pathway through which olanzapine inhibits GLUT4 membrane transport via the TNF-α/FABP4/Dhhc7 axis, thus ultimately leading to insulin resistance.

Given the role of sex hormones in metabolic regulation, we examined the expression of estrogen (ER), androgen (AR), and progesterone (PR) receptors...The dedifferentiation and browning of adipocytes, altered adipocytokine expression, and increased lactate production observed in hRAN reflect the metabolic stress imposed by the tumor environment. Here, we provide evidence, using an ex vivo model, of a dynamic partnership between human adipose tissue and ccRCC tumors.

Moreover, using an OvCa mouse model, we found that in OvCa mice BMS309403 treatment partially diminished CD8+Tsen formation by reducing FA uptake, and improved anti-tumor immunity, and prolonged the survival time of OvCa mice when combined with chemotherapy. Our work suggests FABP4-mediated FA metabolism as a therapeutic target to counteract T cell senescence in adipocyte-rich TME, providing a novel immunotherapeutic strategy for OvCa.

Notably, we identified PAX3 as a transcriptional target associated with Nrf2 activation, suggesting a potential link between Nrf2 signaling and adipogenic regulation. Together, these findings reveal a previously underappreciated role for Nrf2 in human adipogenesis.

FABP4 is a promising independent prognostic biomarker for EOCRC, associated with an immunosuppressive microenvironment and maybe a potential guidance for immunotherapy and chemotherapy selection. Further multi-center prospective studies are warranted to validate its clinical utility.

In TNBC cells, both normal- and adjacent-CM partially shifted MDA-MB-231 morphology toward a more epithelial-like state, decreasing caveolin-1 levels, while adjacent-CM increased MMP9 expression. Overall, these results reveal that adipose tissue-derived soluble factors exert significant and subtype-dependent effects on BC tumorigenicity.

This study systematically delineates a novel panel of early-detection biomarkers for CRC and identifies SB-225002 as a repurposed candidate therapeutic agent. The integrative strategy combining multi-cohort transcriptomic analysis, drug-repositioning platforms, molecular docking, and experimental validation offers a feasible framework for discovering clinically actionable biomarkers and small-molecule therapies for CRC.

The area under the curve for ILK was calculated to be 0.687 (95% CI: 0.600-0.773), while for FABP4, it was 0.638 (95% CI: 0.548-0.728). The current research demonstrates that the positive expression of ILK and FABP4 is significantly linked to the pathogenesis, clinical manifestations, pathological characteristics, biological behaviors, and unfavorable prognosis in EHCC.

This study is the first to demonstrate that metformin mitigates diabetic renal senescence by simultaneously targeting the FABP4/FOXO1 axis and immunometabolic enzymes SDH and ACLY. These findings highlight the translational significance of metformin as a prototype for immunometabolic and immunosenescence-directed therapies in DN.

CD36⁺ CAFs drive immunosuppressive metabolic reprogramming via the OxLDL-PPARG-ANGPTL4 axis, promoting CD8⁺ T cell exhaustion and resistance to immunotherapy in osteosarcoma. Targeting this pathway with VitE alleviated CAF-mediated immune suppression and enhanced PD-1 blockade responses in preclinical models, providing a rationale for metabolism-based combinatorial strategies in osteosarcoma.

This review focuses on the role of FABP4 in tumors and systematically elucidates the specific mechanisms through which FABP4 regulates lipid metabolism and alters the tumor microenvironment. This review also provides an in-depth analysis of the complex network relationship between FABP4-mediated lipid metabolism and the tumor microenvironment and reveals the critical role of FABP4 in tumor occurrence, development, and metastasis, offering a new theoretical basis and potential targets for tumor therapy.

We developed an anti-FABP4 neutralizing antibody that successfully inhibited FABP4-driven CSC functions and suppressed MASLD-induced HCC. In conclusion, our findings indicate that adipocyte-derived FABP4 plays a critical role in the development of MASLD-induced HCC and targeting the ITGB1/PI3K/AKT/β-catenin signaling cascade may offer a promising approach to combat this aggressive disease.