基础医学论著

脂肪因子Chemerin调节结肠癌细胞系迁移及侵袭能力的机制研究*

  • 王彬 ,
  • 曹登义 ,
  • 王远鹏 ,
  • 李乃树 ,
  • 崔皖晋
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  • 蚌埠医学院第二附属医院,安徽蚌埠 233030
王彬

收稿日期: 2023-07-12

  网络出版日期: 2024-02-29

基金资助

*蚌埠医学院自然科学重点项目(020byzd193)

The mechanism of adipokine Chemerin regulating the migration and invasion of colon cancer cell lines

  • WANG Bin ,
  • CAO Dengyi ,
  • WANG Yuanpeng ,
  • LI Naishu ,
  • CUI Wanjin
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  • The Second Affiliated Hospital of Bengbu Medical College, Bengbu 233030,China

Received date: 2023-07-12

  Online published: 2024-02-29

摘要

目的: 探讨Chemerin对结肠癌细胞侵袭与迁移能力的影响及作用机制。方法: 采用不同浓度的Chemerin(0、100、200、300、400、500 ng/mL)处理结肠癌细胞系HCT116、SW480,通过Transwell法检测细胞的侵袭与迁移能力;以HCT116、SW480细胞为材料进一步研究,分为4组,pEGFP-N1阴性对照组(vector control)、si-Chemerin阴性对照组(si-NC)、pEGFP-N1-Chemerin组与si-Chemerin组,转染后检测各组细胞的侵袭与迁移能力,采用qRT-PCR检测上皮细胞钙黏蛋白(E-cadherin, E-cad)、神经钙黏附蛋白(N-cadherin, N-cad)和波形蛋白(vimentin)mRNA水平,采用Western blot法检测E-cad、N-cad和vimentin蛋白表达水平。结果: 外源性Chemerin可提升结肠癌细胞HCT116、SW480侵袭率与迁移数(P<0.05),且存在剂量依赖性,细胞迁移数与侵袭率pEGFP-N1-Chemerin组>vector control组、si-NC组>si-Chemerin组(P<0.05);E-cad mRNA与蛋白表达水平pEGFP-N1-Chemerin组<vector control组、si-NC组<si-Chemerin组(P<0.05);N-cad和vimentin mRNA与蛋白表达水平pEGFP-N1-Chemerin组>vector control组、si-NC组>si-Chemerin组(P<0.05)。结论: Chemerin可能通过调控上皮间充质转化促进结肠癌细胞侵袭与迁移。

本文引用格式

王彬 , 曹登义 , 王远鹏 , 李乃树 , 崔皖晋 . 脂肪因子Chemerin调节结肠癌细胞系迁移及侵袭能力的机制研究*[J]. 包头医学院学报, 2024 , 40(2) : 8 -13 . DOI: 10.16833/j.cnki.jbmc.2024.02.002

Abstract

Objective: To investigate the effect of Chemerin on the invasion and migration of colon cancer cells and its mechanism. Methods: Colon cancer cell lines HCT116 and SW480 were treated with different concentrations of Chemerin (0, 100, 200, 300, 400, 500 ng/mL), and the invasion and migration ability of cells were detected by Transwell method. HCT116 and SW480 cells were further studied and divided into 4 groups: pEGFP-N1 negative control group (vector control), si-Chemerin negative control group (si-NC), pEGFP-N1-Chemerin group and si-Chemerin group. After transfection, the invasion and migration ability of each group was detected. The mRNA levels of E-cadherin (E-cad), N-cadherin (N-cad) and vimentin were detected by qRT-PCR, and the protein levels of E-cad, N-cad and vimentin were detected by Western blot. Results: Exogenous Chemerin increased the invasion rate and migration number of colon cancer cells HCT116 and SW480 (P<0.05), which was dose-dependent, and cell migration number and invasion rate in pEGFP-N1-Chemerin group>vector control group, si-NC group>si-Chemerin group (P<0.05). The expression levels of E-cad mRNA and protein in pEGFP-N1-Chemerin group<vector control group, si-NC group<si-Chemerin group (P<0.05). The mRNA and protein expression levels of N-cad and vimentin in pEGFP-N1-Chemerin group>vector control group, si-NC group>si-Chemerin group (P<0.05). Conclusion: Chemerin may promote colon cancer cell invasion and migration by regulating epithelial-mesenchymal transition.

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