Pivotal contribution of super-enhancer-driven KLF6 expression to the adipogenesis of human adipose-derived stem cells.
Nguyen MP., Yamagata K., Nguyen AP., Zhang T., Sakai H., Ngo UT.
Laboratory Study, published in Inflamm Regen (2026) — 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
- Inflamm Regen (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41549316
- PMCID
- PMC12829020
- DOI
- 10.1186/s41232-026-00406-8
Abstract (original English)
Background Super-enhancers (SEs), characterized by dense clusters of enhancer elements enriched with transcriptional activator binding sites, are involved in cell differentiation. However, little is known about SE-mediated regulation of adipogenic genes. The aim of this study was to elucidate the functional role of the KLF6-proximal SE during the adipogenesis of human adipose-derived stem cells (hADSCs). Methods Adipogenic induction medium (AIM) was used for differentiation of hADSCs into adipocytes, which were evaluated for adipogenic gene expression and adipogenesis using quantitative PCR and Oil Red O (ORO) staining, respectively. The effects of SE inhibitors, locked nucleic acid-mediated enhancer RNA (eRNA) knockdown, and small interfering RNA-mediated knockdown of KLF6 on adipogenesis and adipogenic gene levels were evaluated. Chromatin immunoprecipitation assays were performed to identify transcriptional regulators binding to the promoter regions of KLF6 and the adipogenesis-inhibitory Delta-like non-canonical Notch ligand 1 (DLK1) gene during adipogenesis. Results In silico screening identified KLF6 as an obesity-susceptibility gene associated with single-nucleotide polymorphisms and located within the domain of SE_00159, which was activated in adipocytes. AIM-cultured hADSCs exhibited time-dependent increases in KLF6 mRNA and protein expression. During adipogenesis, the
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.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.