STAT1 promotes lipid deposition in tumor-associated macrophages in laryngeal cancer tissues by regulating APOL6 expression
10.12007/j.issn.0258-4646.2025.10.010
- VernacularTitle:STAT1通过调控APOL6表达促进喉癌组织中肿瘤相关巨噬细胞脂质沉积
- Author:
Xiaoming LI
1
;
Yuelin WU
;
Zhenming XU
;
Weineng FU
;
Yuanyuan SUN
Author Information
1. 中国医科大学生命科学学院医学遗传学教研室,沈阳 110122
- Publication Type:Journal Article
- Keywords:
STAT1;
APOL6;
laryngeal cancer;
tumor-associated macrophages;
lipid metabolism
- From:
Journal of China Medical University
2025;54(10):919-925
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the molecular mechanism by which STAT1 regulates the expression of APOL6 in order to mediate lipid deposition in tumor-associated macrophages(TAM)in laryngeal cancer tissues.Methods Real-time polymerase chain reaction,Western blotting,immunohistochemistry,and enzyme-linked immunosorbent assays were used to detect the expression levels of STAT1 and APOL6 in laryngeal cancer tissues,as well as the regulatory effect of STAT1 on APOL6 expression.Chromatin immunoprecipitation was used to elucidate the molecular mechanisms underlying APOL6 regulation by ST AT1.Oil Red O staining was used to evaluate the lipid deposition in TAM.Results The expression levels of STAT1 and APOL6 in laryngeal cancer tissues were significantly higher than those in the adjacent normal tissues(P＜0.01).STAT1 transcriptionally activated APOL6 gene expression.STAT1 overexpression sig-nificantly promoted the expression and secretion of APOL6 in laryngeal cancer cells and induced lipid deposition in TAM.Conclusion STAT1 is a novel transcription factor for the APOL6 gene.STAT1 promotes lipid deposition in the TAM of laryngeal cancer tissues by regu-lating APOL6 expression,thereby reshaping the lipid metabolism of TAM.
