PRDM16 (PR/SET Domain 16)

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 results suggest an association of PRDM16 overexpression with the NPM1/FLT3-ITD/DNMT3A triple-mutant AML genotype, typically linked to high leukemia stem cell frequencies and poor prognosis. Importantly, within this adverse AML subtype low PRDM16 expression is an independent prognostic marker for favorable outcome, supporting an anti-leukemic mechanism in AMLs with repressed PRDM16 transcription.

Based on these genes, we also identified several potential therapeutic agents and conducted drug sensitivity analyses. This study elucidated the potential mechanisms of NECSO in LUAD and established an effective prognostic model, offering novel insights for the diagnosis and treatment of LUAD.

ChIP-qPCR further revealed that PRDM16 binds upstream of the promoter of RB1, a potent repressor of E2F activity. Overall, this study developed a straightforward method for inducing cancer cell dormancy and applied this approach to find that PRDM16 governs an intrinsic dormancy program in PCa.

In our population, an increased incidence of severe mucositis was observed in nonmodifiable factors such as sex and renal function. However, the implementation of modifiable factors, including the use of prophylactic G-CSF or antibiotics and administering melphalan over 2 days could diminish the severity of this complication.

The chimera occurs between exon 1 of the PR/SET Domain 16 (PRDM16) gene and exon 2 of the oncogene V-Ski Avian Sarcoma Viral Oncogene Homolog (SKI) gene. The finding provides insight into the role of genetic alterations, including fusion genes, in development and progression of T-PLL and may possibly lead to the development of effective and precise targeted therapy for this disease.

The inhibition of mitochondrial respiration with metformin or tigecycline abrogated AraC resistance in MF9/sPrdm16 cells via an energetic shift toward low OxPHOS status. Together, we showed that PRDM16 overexpression activates mitochondrial respiration through metabolic reprogramming via MYC-SLC1A5-Glutaminolysis axis, thereby conferring AraC resistance on AML cells. These results suggest that targeting mitochondrial respiration might be a novel treatment strategy to overcome chemoresistance in AML patients with high PRDM16 expression.

Integrating Mendelian randomization, multi-omics, and artificial intelligence could reveal novel therapeutic targets. A comprehensive prevention strategy combining lifestyle interventions, pharmacological therapies, and biomarker-driven diagnostics is crucial to reducing obesity-related cancer burden and improving patient outcomes.

PRDM16 expression could be an effective parameter diagnosing and assessing the prognosis of LUAD. Serum PRDM16 may be a convenient way to identify LUAD, especially, when PRDM16 is combined with traditional tumor markers.

Despite significant heterogeneity among the included studies and the use of subjective visual methods for phenotype assessment, our review highlights the critical role of fundamental biological processes, such as development and cellular organisation, in skin ageing. Future research that targets the same SNP across multiple populations could strengthen the association of additional loci with skin ageing. Further investigation into these underlying biological processes would significantly advance our understanding of the pathogenesis of skin ageing phenotypes.

Our study first shows that DNA methylation-mediated suppresser role of PRDM16 in CRC progression via PPAR γ/EMT pathway.

The browning effect of CK was nullified by SIRT3 knockdown, suggesting that CK induces beige remodeling of WAT by regulating mitochondrial dynamics and SIRT3 expression. These findings suggest CK's potential as a therapeutic agent for obesity and metabolic disorders that promotes the transformation of WAT into a metabolically active beige phenotype.