FABP5 (Fatty Acid Binding Protein 5)

Combination regimens such as retinoic acid with entinostat and doxorubicin achieve potent antitumor synergy in preclinical models. Notably, emerging methylation-based classifiers that identify retinoid-responsive triple-negative breast cancer subsets, together with the paradoxical pro-tumorigenic effects of stromal RARβ, underscore the novelty and translational significance of integrating tumor-intrinsic and microenvironmental determinants of retinoid sensitivity. Together, these approaches may help re-establish functional retinoid signaling and realize the therapeutic potential of retinoic acid in breast cancer.

Experimentally, GLA inhibited HCC cell proliferation and aggressiveness and promoted cell death-related pathways consistent with anti-tumor activity. Our deep learning-guided workflow identified γ-linolenic acid as a natural FABP5 inhibitor and supports its potential as a lead compound for HCC therapy.

In vitro, treatment with adipose tissue-conditioned medium (ACM) or visceral obesity-associated fatty acids induced lipid droplets accumulation and enhanced METTL27/FABP5/PPARD/CPT1A signaling, exacerbating CRC malignancy. This study is the first to elucidate METTL27's biological function, identifying it as a key upstream partner of FABP5, delineating its regulation of the FABP5/PPARD/CPT1A axis and its role in driving CRC progression in the context of visceral obesity, thereby providing new directions for therapeutic targets in CRC patients with visceral obesity.

Dietary SA can promote CRC via FABP5 without promoting obesity.

Notably, the supplementation of arachidonic acid not only reverses p53-mediated ferroptosis resistance, but also coordinates with p53 to initiate ferroptosis independently of additional oxidative stress, effectively suppressing the growth of CRC cells both in vitro and in vivo. Altogether, our study uncovers that the availability of PUFAs is crucial for p53 to exert a pro-ferroptotic function in CRC.

Furthermore, in TMX1-overexpressing HuH-7 cells, FABP5 knockdown negated the effects of TMX1 overexpression, suggesting that FABP5 mediates TMX1's regulation of HCC cell proliferation. Consequently, this study elucidates the mechanisms by which TMX1 contributes to HCC development, suggesting that TMX1 may serve as a potential biomarker and therapeutic target in the context of HCC.

Notably, inhibition of secretory pathways in remote tumors effectively abrogated these metabolic alterations, with FABP5 in tumor-derived extracellular vesicles identified as a key mediator. These findings uncover a unique aspect of cancer progression mechanisms, implicating tumor-driven systemic lipid metabolic remodeling and vitamin A dysregulation in metastatic progression and therapeutic response.

Simultaneous capture of biomarkers including Lamin-B1, Transferrin receptor protein 1, Fatty acid-binding protein 5, folate receptor 1, and Aminopeptidase N, underscores the method's potential for early diagnosis and prognosis. Overall, DMSN-CS-LA offers an effective enrichment platform, advancing glycoproteomic analysis in cancer research.

Through in silico and database-based validation, biological samples and clinical data confirmed that these genes were significantly overexpressed in HCC (p < 0.001) and were correlated with poor prognosis (p < 0.01). AAI may synergistically activate the PPAR signaling pathway by targeting EZH2, FABP5, and RXRA, driving lipid metabolism reprogramming and promoting the occurrence and development of HCC.

These findings highlight the diagnostic and therapeutic relevance of Kisspeptin-10-associated molecular regulation in GB. This is the first study to integrate transcriptomics, miRNA-mRNA network analysis, and experimental validation to elucidate Kisspeptin-10-mediated modulation of GB progression.

Our findings demonstrate that SBFI-1143 significantly alters the transcriptomic landscape of prostate cancer and may serve as a potentially effective therapeutic option for this disease.

In vitro validation confirmed that ICT suppresses HepG2 and Huh7 cells proliferation and migration in a dose-dependent manner, while molecular analyses demonstrated that ICT treatment significantly downregulates CA9, UCK2, and FABP5 expression and simultaneously upregulates CYP2C9, thereby supporting its role in modulating critical oncogenic pathways. Modulation of ICT-targeted genes was found to effectively suppress HCC progression, underscoring their potential value as prognostic biomarkers and ideal therapeutic targets for the treatment of HCC.