ACAT1 (Acetyl-CoA Acetyltransferase 1)

Building on the above signature, we mined the cMAP repository and retrieved sulfasalazine as an ACAT1-directed small molecule; molecular docking was subsequently employed to assess the predicted binding pose and affinity...Our findings establish ACAT1 as a master regulator of lactate metabolism and protein lactylation in UC pathogenesis. The developed lactylation subtype stratification system and elucidated immune-stromal interaction network provide novel mechanistic insights, positioning ACAT1 as a potential diagnostic biomarker and therapeutic target for precision UC management.

This SOX10-TAF15 complex subsequently enhanced ACAT2 protein levels, stimulated cholesterol synthesis, suppressed apoptosis, and ultimately drove melanoma proliferation. Our findings reveal that the SOX10-TAF15-ACAT2 axis is a key regulator of cholesterol synthesis and melanoma proliferation, presenting a promising therapeutic target.

Chemosensitivity analysis showed that the high-risk group had increased sensitivity to four drugs, including Axitinib, but decreased sensitivity to 21 drugs, including Cisplatin...Molecular docking revealed that five compounds, including Oseltamivir, could bind directly to NEU1. Knockdown of NEU1 significantly reduced proliferation, migration, and invasion of LIHC cells, and slowed LIHC tumor growth. We constructed a histone acetylation-based risk model for LIHC diagnosis, prognosis, and therapy, identifying NEU1 as a key biomarker and potential therapeutic target.

The present study underscores the pivotal function of ACAT2 in CC progression and delineates its potential as a therapeutic latent strategy. This approach involves the strategic obstruction of the metabolic pathway associated with ACAT2.

Notably, we highlight the potential regulatory role of ANK2 in the progression of CRC. This research provides theoretical support and new directions for early screening, diagnostic biomarker identification, and targeted therapy strategies for CRC.

This study is the first to analyze the regulatory network of palmitoylation in HCC epithelial cells by combining single-cell and bulk transcriptomes, providing new molecular targets and methodological references for HCC prognosis evaluation and precision therapy.

Notably, combining circUBR5-targeting antisense oligonucleotides with cisplatin synergistically inhibited tumor growth and reversed chemoresistance in vivo. Thus, circUBR5 promotes GSRCC progression through dual pathways coordinating estrogen signaling and cholesterol metabolism, and its exosomal dissemination facilitates chemoresistance induction within the tumor microenvironment, highlighting its potential as a prognostic biomarker and therapeutic target.

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.

Although rare, neuroendocrine GBC was separately characterized, revealing MEIS1 as a potential regulator of neuroendocrine-like features. Together, this study establishes a proteogenomic landscape of GBC, providing biological insights and guiding future translational efforts.

On the other hand, doxorubicin treatment upregulated ACAT1 and ADCY3, while a slight downregulation was observed in NME2. These molecular changes suggest that G. lucidum induces apoptosis and impairs cancer cell proliferation through metabolic disruption and gene modulation.

Notably, targeting this axis with the SIRT6 inhibitor OSS-128167 combined with CAPZA1 depletion significantly suppresses ccRCC cell growth. Our study reveals a PAT-derived lipid metabolite-fuelled signaling cascade that reprograms lipid metabolism in ccRCC, identifying CAPZA1/USP48/SIRT6 as actionable therapeutic targets for metabolic malignancies.

In conclusion, metabolic engineering, leveraging its impact on epigenetic regulation during CAR T cell manufacturing, is crucial for generating potent, persistent, and functionally resilient products. This approach holds immense promise for expanding the curative potential of CAR T cell therapy to a broader range of cancers, particularly challenging solid tumors.