FABP5 (Fatty Acid Binding Protein 5)

We developed a stemness-associated four-gene signature that enables risk stratification in GBM and reveals an immunosuppressive microenvironment in high-risk tumors, providing new directions for prognosis and targeted therapy.

Importantly, silencing astrocytic Fabp5 effectively rescued oligodendrocytes from this oxidative injury and cell death. These findings establish astrocytic FABP5 as a central regulator linking glial inflammation to oligodendrocyte susceptibility, highlighting it as a promising therapeutic target for MSA.

Using doxycycline-inducible shRNA constructs in HD-MB03 cells (a MYC-amplified Group MB model) to achieve SMARCA4 knockdown, we applied quantitative mass spectrometry to profile the resulting proteomic changes...The overexpression of top candidates like SMARCA2, CRABP2, FABP5, TAGLN2, CYP27A1, and SCP2 was validated in a separate validatory set. Our study reveals the proteomic landscape of Group 3 medulloblastoma following SMARCA4 loss, highlighting novel therapeutic targets for functional validation and exploitation.

These findings suggest that early HPV11 entry is associated with FABP5-mediated lipid metabolic alterations and that FABP5 represents a promising host factor for further validation. Our study demonstrates that inhibition of FABP5 reduces HPV11 PsV infection readouts, indicating that targeting FABP5 may provide a novel strategy for the prevention and treatment of HPV infection.

This study identified distinct expression patterns of FABPs across breast cancer subtypes and highlighted their potential roles in immune modulation. These findings offer new insights into the diverse functions of FABPs in breast cancer and their implications for prognosis.

In vivo, FABP5 depletion suppressed tumor growth, promoted CD8+ T cell differentiation, and reduced PGE2, mPGES-1, PD-L1, and PCNA expression in tumor tissues. Collectively, these findings demonstrate that FABP5 depletion inhibits PCa proliferation and alleviates immune suppression by activating CD8+ T cells, highlighting FABP5 as a potential therapeutic target for CRPC.

Metabolic subtyping identifies DEMs as critical drivers of glioma progression. The DEM-derived risk model, combined with EGFR/IDH status, provides a clinically actionable tool for prognosis and targeted therapy development.

Our integrative approach identifies CDH17 and HOXC13 as biologically relevant, stage-associated prognostic biomarkers in UM. These findings provide a foundation for mechanistic studies and potential translational applications, including therapeutic targeting and risk-stratified patient management.

The MR analysis in this study revealed that genetic alterations in AS were significantly associated with a reduced risk of lung cancer. Transcriptomic data indicated that chronic inflammation linked AS and lung cancer: inflammatory mediators drove AS yet restrained lung cancer progression in the tumor microenvironment, while AS-derived immune molecules and pathways further suppressed tumor growth.

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.