CPT1A (Carnitine Palmitoyltransferase 1A)

TFE3 fusion proteins enhance FAO and drive TFE3 rRCC progression via the PGC-1α/PPARα/CPT1A axis. Targeting CPT1A could inhibit tumor cell proliferation, suggesting that this pathway may serve as a potential therapeutic target for TFE3 rRCC.

In summary, CD38 functions as both a metabolic regulator and an immunologic checkpoint, coordinating suppressive networks and shaping iNKT cell fate. These multifaceted roles position CD38 as a transformative target for next-generation immunotherapies.

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.

In vitro experiments further showed that DEHP and MEHP promote the proliferation and migration of breast cancer cells (MCF-7 and MDA-MB-231), enhance lipid accumulation and mitochondrial function, and validate the altered expression of these prognostic genes at the transcriptional level, with MEHP exerting more pronounced effects. In conclusion, this study suggests that DEHP and MEHP may activate metabolic reprogramming in breast cancer, thereby contributing to disease progression and poorer prognosis, highlighting these genes as potential prognostic biomarkers and therapeutic targets.

Notably, cg20370568, a cis-expression quantitative trait methylation site for ANTXR2, mediates 20% of the effect of body-trunk-radiotherapy on abnormal glucose. These findings suggest that prior genotoxic cancer treatments may become biologically embedded through DNAm variations that could contribute to cardiometabolic dysfunction and highlight candidate biomarkers for refining risk stratification and guiding intervention strategies in survivorship care.

Our study reveals that GBA harbors malignant potential at both epithelial and immune microenvironmental levels. The expression of CCL20, CCL5, and PRDX1 may serve as molecular markers for stratifying high-risk GBA, while PRDX1 represents a promising therapeutic target for reprogramming the tumor immune microenvironment in GBC.

Importantly, CEBPB expression and enhancer activation were not modulated by VHL status and it could be targeted pharmacologically. The CEBPB-GPD1L-ether lipid-Akt-CPT1A axis is proposed as a new druggable driver in ccRCC integrating epigenetics, transcription, intermediary metabolism and oncogenic signaling.

We elucidated the relationship between UC and hypoxia/mitophagy and identified potential diagnostic biomarkers. This study provides a reference for the future development of targeted treatment strategies to improve diagnostic and therapeutic protocols for UC.

Among 17 patients in the DLBCL group, 6 received epirubicin chemotherapy with an average dose of 59.28 ± 12.54 mg/m2 per cycle, and 11 received liposomal doxorubicin chemotherapy with an average dose of 25.21 ± 3.14 mg/m2 per cycle...Alterations of myocardial metabolism monitored by 18F-FDG PET/CT may represent early indicators of metabolic remodeling, potentially identifying patients at risk for AIC. https://www.chictr.org.cn/, identifier ChiCTR2400088740.

Specifically, AdipoRon preferentially suppressed ACC1 expression and subsequently downregulated CPT1A, indicating disruption of fatty acid metabolism. These findings establish that AdipoRon suppresses MM progression through AMPK-driven metabolic reprogramming and apoptosis induction, positioning adiponectin receptor agonism as a promising therapeutic strategy for multiple myeloma.

Inhibition of RACGAP1 sensitized TNBC cells to ferroptosis by inhibiting CPT1A-mediated FA metabolism. Targeting RACGAP1 might be feasible strategy for TNBC management.

In vitro mechanistic studies revealed that CPT1A may promote mitochondrial damage and induce cardiomyocyte injury by interacting with Parkin. This study underscores the utility of multi-omics integration in elucidating TIC mechanisms and paves the way for personalized cardioprotective strategies in HER2-targeted therapy.