摘要： 目的 探讨半乳糖凝集素3（Gal-3）低表达对肝癌HepG2细胞增殖的影响及作用机制。方法 将细胞分为siRNA干扰组（转染靶向Gal-3的siRNA）、阴性对照组（转染阴性siRNA）和空白对照组（仅加转染试剂）。转染48 h后，采用实时qPCR和Western blotting在mRNA和蛋白水平进行抑制效果鉴定。MTT法检测Gal-3表达抑制后对细胞增殖活力的影响；Western blotting检测各组细胞增殖细胞核抗原（PCNA）、蛋白激酶（Akt）、磷酸化Akt（p-Akt）、哺乳动物雷帕霉素靶蛋白（mTOR）及磷酸化mTOR（p-mTOR）蛋白的表达。结果 Western blotting和实时qPCR检测结果显示，siRNA干扰组Gal-3表达较阴性对照组和空白对照组均显著降低（P < 0.05）。与阴性对照组和空白对照组比较，siRNA干扰组细胞增殖活力，PCNA、p-Akt及p-mTOR表达明显下调（P < 0.05）；而Akt、mTOR表达无统计学差异（P > 0.05）。结论 Gal-3低表达抑制肝癌HepG2细胞增殖，其作用机制可能是通过抑制PI3K/Akt/mTOR信号转导通路来实现的。

半乳糖凝集素3低表达对肝癌细胞增殖的影响及作用机制

吴雪艳¹, 赵依纳², 王小杰³, 李美川⁴, 李欣³

1. 承德医学院人体解剖学教研室, 河北 承德 067000;
2. 河北生殖妇产医院生殖医学科, 石家庄 050000;
3. 承德医学院组织与胚胎学教研室, 河北 承德 067000;
4. 承德医学院基础医学研究所, 河北 承德 067000

收稿日期:2019-11-12出版日期:2020-10-30发布日期:2020-10-13
通讯作者:李欣E-mail:hbcdlx@cdmc.edu.cn
作者简介:吴雪艳(1983-),女,讲师,硕士.
基金资助:河北省高等学校科学研究计划（ZD2018058）


关键词: 半乳糖凝集素3, 低表达, 肝癌细胞, 增殖
Abstract: Objective To investigate the effect and mechanism of low expression of galectin 3 (Gal-3) on the proliferation of human hepatocellular cancer (HepG2) cells. Methods HepG2 cells were divided into siRNA interference,negative control,and blank control groups. Using liposome transfection,siRNA targeted to Gal-3 and negative siRNA were transfected into the siRNA interference and negative control groups,respectively. Transfection reagent was added in the blank control group. After 48 h of transfection,inhibitory effects were identified at the mRNA and protein levels with RT-qPCR and western blotting,respectively. The MTT assay was used to detect the effect of low expression of Gal-3 on proliferation of HepG2 cells. Western blotting was used to detect the expression levels of proliferating cell nuclear antigen (PCNA),protein kinase (Akt),p-Akt,mammalian target of rapamcycin (mTOR),and p-mTOR. Results Western blotting and RT-qPCR results showed that the expression of Gal-3 in the siRNA interference group was significantly lower than that in the negative control and blank control groups (P < 0.05). The proliferation activity and expression of PCNA,p-Akt,and p-mTOR of the siRNA interference group were significantly decreased compared to the negative control and blank control groups (P < 0.05). However,there was no statistically significant difference in the expression of Akt and mTOR amongst these groups (P > 0.05). Conclusion Low expression of Gal-3 prevents the proliferation of HepG2 cells by inhibiting the PI3K/Akt/mTOR signaling pathway.
Key words: galectin 3, low expression, hepatocellular cancer cell, proliferation
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