目的：探究长链非编码RNA（lncRNA）结肠癌相关转录因子1（CCAT1）靶向miR-375-3p 通过线粒体途径诱导人口腔癌SAS细胞凋亡的作用。方法：人口腔癌SAS细胞随机分为空白组、CCAT1 下调组、CCAT1 上调组、CCAT1 下调对照组、CCAT1 上调对照组、miR-375-3p 下调组、miR-375-3p 上调组、miR-375-3p 下调对照组和miR-375-3p 上调对照组。转染48 h 后，流式细胞术检测细胞凋亡；RT-qPCR 检测miR-375-3p 表达、线粒体凋亡通路相关的基因半胱氨酰天冬氨酸特异性蛋白酶3（caspase-3）、半胱氨酰天冬氨酸特异性蛋白酶9（caspase-9）、β淋巴细胞瘤-2（Bcl-2）和Bcl-2 相关X蛋白（Bax）的mRNA表达；免疫印迹检测caspase-3、caspase-9、Bcl-2、Bax 蛋白表达；双荧光素酶报告实验分析CCAT1 与miR-375-3p 的靶向关系。结果：与空白组和CCAT1 下调对照组比较，CCAT1 下调组细胞凋亡率、miR-375-3p 表达、caspase-3、caspase-9、Bax mRNA 及蛋白表达升高， Bcl-2 mRNA 及蛋白表达降低；与空白组和CCAT1 上调对照组比，CCAT1 上调组细胞凋亡率、miR-375-3p 表达、caspase-3、caspase-9、Bax mRNA 及蛋白表达降低，Bcl-2 mRNA 及蛋白表达升高；与空白组和miR-375-3p 下调对照组比较，miR-375-3p 下调组细胞凋亡率、miR-375-3p 表达、caspase-3、caspase-9、Bax mRNA 及蛋白表达降低，Bcl-2 mRNA 及蛋白表达升高；与空白组和miR-375-3p 上调对照组比较，miR-375-3p 上调组细胞凋亡率、miR-375-3p 表达、caspase-3、caspase-9、Bax mRNA 及蛋白表达升高，Bcl-2 mRNA 及蛋白表达降低。双荧光素酶实验结果提示CCAT1 可靶向调控miR-375-3p。结论： CCAT1 可抑制人口腔癌SAS细胞凋亡，推测是通过靶向抑制miR-375-3p 的表达，调控线粒体凋亡通路相关基因及蛋白的表达来实现的。

Objective ： To explore the role of long chain non-coding RNA（ lncRNA） colon cancer-relatedtranscription factor 1 （CCAT1） targeting miR-375-3p in inducing the apoptosis of human oral cancer SAS cellsthrough mitochondrial pathway. Methods ： Human oral cancer cell line SAS cells were randomly divided intoblank group， CCAT1 down-regulated group， CCAT1 up-regulated group， CCAT1 down-regulated control group，CCAT1 up-regulated control group， miR-375-3p down-regulated group， miR-375-3p up-regulated group， miR-375-3p down-regulated control group， and miR-375-3p up-regulated control group. After 48 hours of transfection， theapoptosis was detected by flow cytometry. RT-qPCR was used to detect the expression of miR-375-3p and the mRNAexpressions of genes related to mitochondrial apoptosis pathway， such as caspase-3， caspase-9， Bcl-2， and Bcl-2-related X protein （Bax）. The protein expressions of caspase-3， caspase-9， Bcl-2 and Bax were detected by Westernblotting. The targeting relationship between CCAT1 and miR-375-3p was analyzed by dual luciferase reporter assay.Results ： Compared with the blank group and the CCAT1 down-regulated control group， the apoptosis rate， miR-375-3p expression， and mRNA and protein expressions of caspase-3， caspase-9， and Bax in the CCAT1 downregulatedgroup were increased， while the Bcl-2 mRNAand protein expressions were decreased. Compared withthe blank group and CCAT1 down-regulated controlgroup， the apoptosis rate， miR-375-3p expression， andmRNA and protein exprssions of caspase-3， caspase-9， and Bax in the CCAT1 up-regulated group weredecreased，while the Bcl-2 mRNA and protein expressions were increased. Compared with the blank group and the miR-375-3pdown-regulated control group， the apoptosis rate， the expression of miR-375-3p， and mRNA and protein expressionsof caspase-3， caspase-9， and Bax in the miR-375-3p down-regulated group were decreased， while Bcl-2 mRNA andprotein expressions were increased. Compared with the blank group and the miR-375-3p up-regulated control group，the apoptosis rate， the expression of miR-375-3p， the mRNA and protein expressions of caspase-3， caspase-9， Baxwere increased in the miR-375-3p up-regulated group， while the Bcl-2 mRNA and protein expressions were decreased. The dual luciferase reporter assay confirmed that CCAT1 could target miR-375-3p. Conclusion ： CCAT1 can inhibit theapoptosis of human oral cancer SAS cells， which is speculated to be achieved by targeting the expression of miR-375-3p and regulating the expressions of genes and proteins related to the mitochondrial apoptosis pathway.