CAJ | 학술논문

目的探讨组蛋白去乙酰化酶2(HDAC2)表达下调对喉鳞癌Hep-2细胞增殖、细胞凋亡和细胞迁移的影响.方法利用脂质体2000将HDAC2小干扰RNA (siRNA)和对照siRNA转染喉鳞癌Hep-2细胞,将细胞分为3组:未处理组、siRNA对照组和HDAC2 siRNA转染组.利用Westernblot检测转染HDAC2 siRNA后喉鳞癌Hep-2细胞中HDAC2蛋白的表达;利用CCK-8分析3组细胞增殖的变化;采用流式细胞术检测3组细胞凋亡情况;接着利用Boyden小室研究3组细胞迁移能力的变化,最后采用Westem blot研究与细胞凋亡和细胞迁移密切相关蛋白的表达.结果 HDAC2siRNA明显下调喉鳞癌Hep-2细胞中HDAC2蛋白的表达.HDAC2表达下调明显抑制喉鳞癌Hep-2细胞的增殖和诱导细胞凋亡,并抑制喉鳞癌Hep-2细胞的迁移.此外,HDAC2表达下调明显增加caspase-3和caspase-9的表达,但降低基质金属蛋白酶(MMP)-2和MMP-9的表达.结论 HDAC2可能在喉鳞癌发生发展中发挥重要作用,其表达下调介导的细胞凋亡和迁移抑制可能与caspase-3和caspase-9表达的升高以及MMP-2和MMP-9表达的降低相关.
목적 탐토조단백거을선화매2(HDAC2)표체하조대후린암Hep-2세포증식、세포조망화세포천이적영향.방법 이용지질체2000장HDAC2소간우RNA (siRNA)화대조siRNA전염후린암Hep-2세포,장세포분위3조:미처리조、siRNA대조조화HDAC2 siRNA전염조.이용Westernblot검측전염HDAC2 siRNA후후린암Hep-2세포중HDAC2단백적표체;이용CCK-8분석3조세포증식적변화;채용류식세포술검측3조세포조망정황;접착이용Boyden소실연구3조세포천이능력적변화,최후채용Westem blot연구여세포조망화세포천이밀절상관단백적표체.결과 HDAC2siRNA명현하조후린암Hep-2세포중HDAC2단백적표체.HDAC2표체하조명현억제후린암Hep-2세포적증식화유도세포조망,병억제후린암Hep-2세포적천이.차외,HDAC2표체하조명현증가caspase-3화caspase-9적표체,단강저기질금속단백매(MMP)-2화MMP-9적표체.결론 HDAC2가능재후린암발생발전중발휘중요작용,기표체하조개도적세포조망화천이억제가능여caspase-3화caspase-9표체적승고이급MMP-2화MMP-9표체적강저상관.
Objective To investigate the effects of historne deacetylase 2 (HDAC2) expression oncell proliferation,apoptosis and migration of laryngeal squamous cell carcinoma (LSCC) Hep-2 cells.Methods HDAC2 siRNA and control siRNA were transfected into LSCC Hep-2 cells by lipofectamine 2000,and cells were divided into three experimental groups:untreated group,control siRNA group and HDAC2 siRNA transfection group.Western blotting was utilized to detect the expression of HDAC2 protein in Hep-2 cells.Cell proliferation and apoptosis were investigated by CCK-8 kit and flow cytometry,respectively.Boyden chamber was used to study cell mnigration.Expressions of cell apoptosis and cell migration related proteins were detected by Western blotting.Results HDAC2 siRNA significantly downregulated the expression of HDAC2 protein in LSCC Hep-2 cells.Down-regulation of HDAC2 expression coincided with an inhibition of cell proliferation and migration along with an induced cell apoptosis of Hep-2 cells.Moreover,down-regulation of HDAC2 expression significantly increased the expressions of caspase-3 and caspase-9 proteins but decreased the expressions of matrix metalloproteinases (MMP)-2 and MMP-9 proteins.Conclusions HDAC2 may play a pivotal role in the initiation and development of LSCC.Downregulation of HDAC2 expression mediates cell apoptosis.Cell migration inhibition may be tightly associated with overexpression of caspase-3 and caspase-9 along with down-regulation of MMP-2 and MMP-9 expressions.