Epigenetic disruption of adipogenic gene enhancers in dedifferentiated liposarcomas and its therapeutic value.
Hattori N., Takamatsu H., Iida N., Asano N., Yamashita S., Oba GM.
Laboratory Study, published in Front Oncol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Front Oncol (2025)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40371227
- DOI
- 10.3389/fonc.2025.1419877
Abstract (original English)
Liposarcoma (LPS) is the most common soft-tissue sarcoma in adults, and well-differentiated liposarcoma (WDLPS) and dedifferentiated liposarcoma (DDLPS) are the most frequent subtypes. These LPSs are considered to develop due to disturbances in the adipogenic differentiation of mesenchymal stem cells. However, the molecular mechanisms underlying the disturbances remain unclear. Here, we aimed to identify the mechanism and explore its therapeutic advantages focusing upon their epigenetic alterations, known to be important in differentiation. First, we conducted a genome-wide DNA methylation analysis using 15 LPSs (6 WDLPSs and 9 DDLPSs) and 6 normal adipose tissues. Unsupervised hierarchical cluster analysis using DNA methylation profiles at enhancers classified the samples into the three histological types, whereas analysis using promoters did not. Principal component analysis revealed that normal adipose tissues and WDLPSs were grouped closely, whereas DDLPSs were scattered. Genomic regions hypermethylated in DDLPSs were enriched for enhancers, especially super-enhancers (13.5% of hypermethylated regions and 7.0% of the whole genome), which were located in the genes involved in adipogenesis, such as PPARG2 and its target genes ( FABP4 and PLIN1 ). In addition, marked decreases in PPARG2 and FABP4 expression were confirmed in DDLPSs. Then, treatment of PPARG2 -expressing DDLPS
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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