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目的:研究罗勒多糖对缺氧条件下肝癌细胞MHCC97H和MHCC97L低氧诱导因子1α(HIF-1α)组蛋白甲基转移酶G9a、去甲基化酶JMJD1A的表达及组蛋白H3K9me2甲基化水平的影响,探讨罗勒多糖对肝癌细胞表观遗传学的调节作用。方法:采用二氯化钴(Co Cl2)模拟细胞缺氧,建立肝癌细胞MHCC97H和MHCC97L体外缺氧模型,通过不同浓度罗勒多糖干预24 h,实时荧光定量PCR法检测各组肝癌细胞中HIF-1α、G9a和JMJD1A mRNA表达水平,Western-blot法检测各组肝癌细胞中HIF-1α、G9a、JMJD1A蛋白表达情况及组蛋白H3K9me2甲基化水平。结果:罗勒多糖能下调MHCC97H细胞缺氧条件下HIF-1α、G9a、JMJD1A mRNA和蛋白的表达和组蛋白H3K9me2甲基化水平以及MHCC97L细胞缺氧条件下HIF-1αmRNA和蛋白的表达和组蛋白H3K9me2甲基化水平(P<0.05)。结论:罗勒多糖对缺氧条件下不同转移潜能肝癌细胞MHCC97H和MHCC97L组蛋白H3K9me2甲基化水平均有有调节作用,其中对高转移潜能肝癌细胞MHCC97H组蛋白H3K9me2甲基化的调节与组蛋白甲基转移酶G9a和去甲基化酶JMJD1A有关,而对低转移潜能肝癌细胞MHCC97L组蛋白H3K9me2甲基化的调节可能是通过其他通路发挥作用。
AIM: To investigate the effects of basil polysaccharide on the expression of histone methyltransferase G9a, demethylase JMJD1A and the histone H3K9me2 methylation level in hepatocarcinoma cells MHCC97H and MHCC97L under hypoxic conditions Influence, to study the basil function of basilar polysaccharides on the regulation of liver cancer cells. Methods: Hypoxia model of MHCC97H and MHCC97L cells was established by using cobalt chloride (Co Cl2) to simulate cell hypoxia. HUVECs were treated with different concentrations of basilactose for 24 hours. Real-time quantitative PCR was used to detect the expression of HIF-1α , G9a and JMJD1A mRNA were detected by Western blot. The expression of HIF-1α, G9a and JMJD1A in each group and the histone H3K9me2 methylation level were detected by Western-blot. Results: The results showed that basilain could down-regulate the mRNA and protein expression of HIF-1α, G9a and JMJD1A and the methylation level of H3K9me2 in MHCC97H cells under hypoxia and the expression of HIF-1α mRNA and protein in MHCC97L cells under hypoxia and the expression of histone H3K9me2 Methylation level (P <0.05). CONCLUSION: Basil polysaccharide regulates the methylation of H3K9me2 in HCC cell line MHCC97H and MHCC97L under hypoxic conditions. The regulation of histone H3K9me2 methylation in HCC cell line MHCC97H is similar to that of Histone A G9a is associated with the demethylase JMJD1A, whereas regulation of histone H3K9me2 methylation in low-metastatic potential hepatocarcinoma MHCC97L may play a role through other pathways.