PPARGC1A (PPARG Coactivator 1 Alpha)

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.

Further, hazelnut extract may reduce oxidative stress, contributing to its anti-cancer properties. The extracts could be utilized as functional ingredients in foods and nutraceuticals to assist with cancer prevention and treatment.

Importantly, many of these compounds also inhibit cancer cell intrinsic metabolism by reducing glycolysis, oxidative phosphorylation, lipid synthesis, and amino acid dependent anaplerosis. This review integrates UCP1 biology, natural product mediated thermogenesis, molecular docking evidence, and tumor metabolic suppression, proposing a unified framework in which natural compounds impose coordinated metabolic pressure on cancer through both adipocyte-driven nutrient competition and direct inhibition of tumor metabolism.

These findings establish thyroid function as a causal determinant of pancreatitis susceptibility, identify cell type-specific mechanisms including local thyroid hormone inactivation and metabolic reprogramming, and demonstrate that patient-derived organoids better preserve prognostically favorable metabolic phenotypes than cell lines. Thyroid function represents a potentially modifiable risk factor for inflammatory pancreatic disease.

Sex, follicular nodular disease, and Graves' disease were not significant predictors. Our findings suggest an association between fusion-driven thyroid neoplasia and florid CLT, warranting further investigation.

In this study, six mitochondrial energy metabolism-related prognosis biomarkers (COX7B, PPARGC1B, NDUFA11, PFKFB4, NDUFV2, and NDUFA7) were screened. A risk model was developed to provide a new reference for the prognosis of ccRCC patients.

Drug sensitivity analysis revealed that tyrosine kinase inhibitors (e.g., ceritinib, imatinib) potently inhibited cancer cell lines in the high PC score group, while inhibitors like acalabrutinib were effective in the low PC score group. Expression of hub genes in KIRC patients was validated using a local cohort and single-cell sequencing. We identified key genes regulating PC infiltration in KIRC and proposed a predictive model that effectively identifies high-risk KIRC patients.

This ML-based model using MRGs effectively predicts CRC prognosis, immune microenvironment, and therapeutic response, offering a framework for precision oncology. The 7-gene signature may guide risk stratification and targeted therapy, bridging mitochondrial biology with clinical outcomes.

Moreover, Intralipid treatment suppressed the expression of fibrosis-related genes, including Lh2b (lysyl oxidase-like 2b) and P4ha (prolyl 4-hydroxylase). These findings suggest that Intralipid administration at a developmental stage prior to normal term enhances ovine adipogenic differentiation and lipid accumulation which might be protective to premature infants, but it might slightly induce inflammation in the adipose tissues.

Specifically, EGFR ecDNA stabilizes tumor-associated macrophages in a hypoxia- and metabolism-driven state, reinforcing a reciprocal AREG-EGFR signaling loop with mesenchymal-like tumor cells. Together, these findings uncover a mechanistic link between ecDNA architecture, transcriptional subtypes, and microenvironmental remodeling, offering critical insights for advancing precision oncology in GB.

The study's findings revealed that the hub genes investigated could be possibly vital genes in determining the molecular mechanism of BCBM.

And we successfully developed a predictive model to forecast the response of CRC patients to cetuximab treatment. This study will provide valuable biomarkers for CRC prognosis and help guide more effective therapeutic strategies.