Ghazi Terisha, Nagiah Savania, Dhani Shanel, Chuturgoon Anil A
Discipline of Medical Biochemistry & Chemical Pathology, School of Laboratory Medicine & Medical Science, College of Health Sciences, Howard College Campus, University of KwaZulu-Natal, Durban 4041, South Africa.
Epigenomics. 2020 Jun;12(11):955-972. doi: 10.2217/epi-2019-0284. Epub 2020 Aug 7.
To determine the effect of the food-borne mycotoxin, fusaric acid (FA) on miR-200a, SUV39H1-mediated H3K9me3, genome integrity and apoptosis in human liver (HepG2) cells and C57BL/6 mice livers. MiR-200a, Sirt1, SUV39H1-mediated H3K9me3, genome integrity and apoptosis was measured in HepG2 cells and C57BL/6 mice livers using qPCR, western blot, DNA electrophoresis and luminometry. FA: upregulated miR-200a and decreased Sirt1 expression in HepG2 cells and mice livers; decreased expression of SUV39H1 and , thus decreasing H3K9me3 and increasing H3K9me1; increased cell mortality via apoptosis. FA induced apoptosis by upregulating miR-200a and decreasing SUV39H1-mediated H3K9me3 in HepG2 cells and mice livers.
为了确定食源性霉菌毒素富马酸(FA)对人肝癌(HepG2)细胞和C57BL/6小鼠肝脏中miR-200a、SUV39H1介导的H3K9me3、基因组完整性和细胞凋亡的影响。使用qPCR、蛋白质免疫印迹、DNA电泳和发光测定法在HepG2细胞和C57BL/6小鼠肝脏中检测miR-200a、Sirt1、SUV39H1介导的H3K9me3、基因组完整性和细胞凋亡。FA:上调HepG2细胞和小鼠肝脏中的miR-200a并降低Sirt1表达;降低SUV39H1的表达,从而减少H3K9me3并增加H3K9me1;通过细胞凋亡增加细胞死亡率。FA通过上调HepG2细胞和小鼠肝脏中的miR-200a并降低SUV39H1介导的H3K9me3诱导细胞凋亡。