CPT2 (Carnitine Palmitoyltransferase 2)

High SOX8 expression promotes EnzR in PCa, suggesting SOX8 as a potential therapeutic target. Our findings demonstrate that SOX8 drives EnzR by activating the SOX8/CPT2 axis, thereby inducing lipid metabolic reprogramming in PCa cells.

Deep learning-derived CTBC metrics, especially VAT/SAT ratio, enhance prognostic stratification beyond TNM staging in locally advanced gastric cancer. This ratio captures a systemic and tumor-level immunometabolic phenotype marked by mitochondrial dysfunction and immune suppression. Our findings highlight VAT/SAT as a noninvasive, clinically actionable biomarker to guide personalized therapy and risk-adapted algorithm in gastric cancer management.

Drug sensitivity analysis indicated that high-risk individuals might be more responsive to chemotherapy, particularly temozolomide and carmustine. This study underscores the prognostic role of the FAM-related risk model for LGGs. Assessing patient risk scores through this model could help tailor personalized treatments, providing valuable guidance for clinical decision-making.

EGCG supplementation in goat semen extenders has a protective effect on post-thawed sperm by improving motility and viability and supporting mitochondrial and apoptotic pathways. These results suggest that EGCG can be a valuable additive for enhancing artificial insemination outcomes in goats.

Collectively, this study elucidates the molecular mechanism by which the HAND1/c-MET axis regulates EC progression through the modulation of FAO. This provides a novel perspective for understanding the pathogenesis of EC and offers potential biomarkers for developing novel diagnostic and therapeutic strategies for EC.

This study utilized LC-MS/MS to systematically profile the proteomic, phosphoproteomic, and metabolomic characteristics of MIBC, NMIBC, and adjacent noncancerous tissues, with the aim of identifying key molecules and metabolites driving bladder cancer progression. Our findings indicate that aberrant phosphorylation of regulatory proteins such as SLC4A7 and MYO9B may play a critical role in mediating the invasive phenotype of MIBC. In parallel, the upregulation of CPT2 and its associated metabolites (e.g., palmitic acid) suggests that lipid metabolic reprogramming, including enhanced β-oxidation and membrane phospholipid synthesis, may contribute to the malignant transition from NMIBC to MIBC. Overall, this study not only reveals potential molecules and metabolites driving bladder cancer progression but also provides a valuable reference for further exploration of pathways associated with bladder cancer invasiveness.

CPT2 knockdown yielded opposite results. CPT2 is a potential prognostic marker of CCA, a tumor suppressor gene to inhibit the malignant progression of CCA, and therefore a potential therapeutic target.

Moreover, we found that SLC25A42 reprograms lipid metabolism in GC cells by upregulating the acetylation and thus the expression of CPT2. Collectively, our data reveal a critical oncogenic role of SLC25A42 in GCs and suggest that SLC25A42 represent a promising therapeutic target for GC.

These results suggest that, the involvement of adaptive metabolic pathways is different depending on the aetiology of HCC. Moreover, the dogma that simultaneous activation of FAO and DNL is incompatible in cancer would not apply to MASLD-HCC.

We found that cortisol treatment sustained OCR by enhancing fatty acid and glutamine metabolism through upregulation of CPT2 and GLS, respectively, to support M2 polarization. Thus, our findings unfold a novel mechanism of immune suppression by cortisol and open avenues for preventive and therapeutic interventions.

In summary, our results suggest that CPT2 acts as a tumor suppressor in the development of ccRCC through the ROS/PPARγ/NF-κB pathway. Moreover, CPT2 is a potential therapeutic target for increasing sorafenib sensitivity in ccRCC.

Steatohepatitic HCC (SH-HCC), characterized by the presence of fat accumulation in tumor cells, ballooned tumor cells, Mallory-Denk body, interstitial fibrosis, and intratumor immune cell infiltration, may represent a metabolic reprogramming for adapting to a lipid-rich tumor microenvironment by downregulating CPT2 and leveraging its intermediates as an "oncometabolite." Genome-wide analyses suggested that SH-HCC may be more responsive to ICIs given its mutual exclusiveness with β-catenin mutation/activation that promotes immune evasion. Thus, further understanding of NAFLD-specific hepatocarcinogenesis and HCC would enable us to improve the current daily practice and eventually the prognoses of patients with NAFLD.