MiR-497通过下调XIAP诱导肝细胞癌LM3的凋亡
MIR-497 INDUCES HEPATOCELLULAR CARCINOMA CELL LM3 APOPTOSIS THROUGH DOWNREGULATING XIAP
刘溪涛1
作者信息
- 1. 内蒙古医科大学附属医院,内蒙古 呼和浩特 010050
- 折叠
摘要
目的 MiR-497在细胞行为中扮演着重要的角色,MiR-497可以与X连锁凋亡抑制蛋白(XIAP)3'-UTR相结合,共同在肝癌细胞的增殖和凋亡中起重要的作用.本研究探讨并验证MiR-497和XIAP在影响肝癌细胞增殖和细胞凋亡中的作用.方法 选取2017年12月至2023年3月内蒙古医科大学附属医院75例原发性肝癌的患者作为研究对象.通过检测肝脏肿瘤组织和癌旁组织标本中MiR-497和XIAP的表达,将正常肝组织L02细胞与肝细胞癌组织LM3细胞中的MiR-497和XIAP水平进行比较.Ki-67蛋白表达及细胞凋亡通过流式细胞仪进行检测.MiR-497和XIAP之间的目标关系通过双荧光素酶报告基因检测进行验证分析.肝细胞癌组织中的LM3细胞可以被分为 mimic NC,miR-97 mimic,si-NC,si-XIAP 和 miR-497 mimic+si-XIAP group.恶性细胞生长能力通过集落形成进行了评价.结果 在肝细胞癌组织与癌旁组织对比中发现,MiR-497明显下调而XIAP的表达却明显增强.在肝癌组织中LM3细胞与正常肝组织中L02细胞相比中发现MiR-497下降而XIAP是升高的.肝癌组织中LM3细胞表现出细胞增殖增强和细胞凋亡减少的特性,并且在肝癌组织LM3细胞中MiR-497可以靶向调控XIAP基因.MiR-497显著的上调和/或XIAP显著降低都弱化了肝癌组织中LM3细胞的增殖和恶性生长,促使Caspase-3和Caspase-7酶活性升高,并促进细胞凋亡.结论 在肝细胞癌组织与癌旁组织相比较中,MiR-497异常下调,而XIAP却是增强的.MiR-497也许可以通过靶向抑制XIAP的表达拮抗在Caspase酶活性中XIAP的抑制作用,从而促进肝癌细胞凋亡.
Abstract
Objective MiR-497 plays a significant role in cell behavior.Bioinformatics analysis showed that miR-497 can bind with the3-UTR of X-linked inhibitor of apoptosis protein(XIAP).This study investigated the role of miR-497 and XIAP in affecting hepatocellular carcinoma(HCC)cell proliferation and apoptosis.Methods There were 75 HCC patients be-tween December 2017 and March 2023 in our hospital enrolled in this study.Tumor tissue and para-carcinoma tissue speci-mens were collected to test miR-497 and XIAP expression.MiR-497 and XIAP levels in normal liver L02 cells and HCC LM3 cells were compared.Ki-67 protein expression and cell apoptosis were detected by flow cytometry.The target relationship be-tween miR-497 and XIAP was verified dual luciferase reporter assay.LM3 cells were divided into mimic NC,miR-497 mimic,si-NC,si-XIAP,and miR-497 mimic+si-XIAP group.Malignant cell growth ability was evaluated by colony formation.Re-sults MiR-497 significantly downregulated,while XIAP expression obviously enhanced in HCC tissue compared with para-carcinoma tissue.MiR-497 reduced and XIAP elevated in LM3 cells compared with L02 cells.LM3 cells presented enhanced cell proliferation and reduced apoptosis.MiR-497 targeted regulated XIAP gene in LM3 cells.MiR-497 upregulation and/or XIAP reduction markedly weakened LM3 cell proliferation and malignant growth,elevated Caspase-3 and Caspase-7 enzyme activity,and promoted cell apoptosis.Conclusions MiR-497 abnormally downregulated,while XIAP enhanced in HCC tis-sue compared with para-carcinoma tissue.MiR-497 may antagonize the inhibitory effect of XIAP on Caspase enzyme activity through targeted suppressing XIAP expression,thus to promote HCC cell apoptosis.
关键词
MiR-497/XIAP/肝细胞癌/细胞凋亡/半胱天冬酶Key words
miR-497/XIAP/liver cancer/apoptosis/Caspase引用本文复制引用
基金项目
内蒙古医科大学附属医院科研项目(NYFYYB010)
出版年
2024
NETL
NSTL
万方数据