ACAT1 (Acetyl-CoA Acetyltransferase 1)

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.

TRIM8 levels are positively correlated with tumor angiogenesis and poor prognosis in gastric cancer patients. These findings elucidate a novel mechanism underlying the upregulation of angiogenesis mediated by K63 ubiquitination-regulated glycolysis in tumor cells and provide a molecular basis for eliminating gastric cancer angiogenesis by targeting TRIM8-dependent PGK1 K63 ubiquitination.

This ACAA1/PI3K/AKT/Nrf2 axis suppresses ferroptosis by regulating redox homeostasis and lipid peroxidation, thereby promoting EC progression. Our findings reveal ACAA1 as a novel regulator of ferroptosis resistance and tumorigenesis in EC, highlighting its potential as a promising therapeutic target for EC treatment.

Western blot and immunohistochemical analyses further demonstrated that HPX upregulates the Bax/Bcl-2 ratio via the TNF-α signaling pathway. This study defines novel molecular subtypes of HCC and reveals that HPX exerts anti-tumor effects through TNF-α-mediated mitochondrial apoptosis, characterized by an increased Bax/Bcl-2 ratio.

The nanodrug effectively reversed the epithelial-mesenchymal transition by inhibiting the PI3K/AKT/mTOR pathway and reversing the hypoxic microenvironment. Furthermore, antitumor immunity was enhanced by elevating the density of CD3+ and CD8+ T cells and triggering macrophage polarization from the M2 to M1 phenotype in tumors.

We also explored the mediating pathways of mitochondrial genes (within the 3-tiers evidence) on prostatic diseases, and identified 8, 4, and 13 metabolites mediating the interaction between mitochondrial genes and BPH, prostatitis, and PCa, respectively, without the involvement of immune characters. These findings highlight the roles of mitochondrial dysfunction-related genes in prostatic diseases and identify key genes and pathways for potential therapeutic targets.

This disruption of lipid homeostasis in clear cell renal carcinoma (pRCC), particularly in mitochondrial cardiolipin metabolism, inhibited mitochondria-dependent apoptosis and, consequently, enhanced tumorigenesis. These findings suggest TRIM59 as a biomarker and potential therapeutic target, supporting precision oncology strategies for pRCC treatment.

This review summarizes the effects and potential mechanisms of cholesterol ester accumulation on cancer cell proliferation, invasion, metastasis, chemotherapy resistance and immune evasion. Additionally, the role of ACAT-1 and the application of its inhibitors in various cancers are discussed, offering novel strategies for cancer therapy and diagnosis.

Moreover, the prognostic signature showed significant correlations with immune landscapes and therapeutic responses, enabling prediction of immunotherapy responsiveness. Collectively, a unique PMRG-based signature effectively predicts prognosis in HCC patients and provides valuable insights into chemotherapy and immunotherapy strategies for these individuals.

Our findings highlight the critical role of the H3K18la/ACAT2/sEV-cholesterol axis in TME reprogramming. Targeting this pathway may improve anti-PD-1 therapy response in pancreatic cancer, providing a novel therapeutic strategy by linking histone lactylation, cholesterol metabolic reprogramming and immune modulation.

In comparison to CHB and NAFLD alone, the prognosis for CHB complicated by NAFLD appears less favorable. This disparity is closely correlated with distinct protein level patterns in the liver following the onset of both diseases. Our study provides novel insights into the disease progression and clinical mechanisms underlying CHB and NAFLD.