[1]马凯,唐国庆,张倩,等.CXCL1在乳癌MCF-7细胞上皮-间质转化中作用[J].齐鲁医学杂志,2017,32(03):253-256.[doi:10.13362/j.qlyx.201703001]
 MA Kai,TANG Guoqing,ZHANG Qian,et al.EFFECT OF CHEMOKINE CXCL1 ON EPITHELIAL-MESENCHYMAL TRANSITION OF BREAST CANCER MCF-7 CELLS[J].Medical Journal of Qilu,2017,32(03):253-256.[doi:10.13362/j.qlyx.201703001]
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CXCL1在乳癌MCF-7细胞上皮-间质转化中作用()
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《齐鲁医学杂志》[ISSN:1008-0341/CN:37-1280/R]

卷:
第32卷
期数:
2017年03期
页码:
253-256
栏目:
出版日期:
2017-08-07

文章信息/Info

Title:
EFFECT OF CHEMOKINE CXCL1 ON EPITHELIAL-MESENCHYMAL TRANSITION OF BREAST CANCER MCF-7 CELLS
文章编号:
1008-0341(2017)03-0253-04
作者:
马凯1唐国庆1张倩2沈若武3付兴芹1张蓓1
1 青岛大学基础医学院免疫学系,山东 青岛 266071; 2 青岛阜外心血管病医院妇产科; 3 青岛大学基础医学院人体形态学实验室
Author(s):
MA Kai TANG Guoqing ZHANG Qian SHEN Ruowu FU Xingqin ZHANG Bei
Department of Immunology, School of Basic Medicine, Qingdao University, Qingdao 266071, China
关键词:
CXC型趋化因子配体1CXC趋化因子受体2乳房肿瘤上皮-间质转化迁移
Keywords:
CXC chemokine ligand 1 CXC chemokine receptor 2 breast neoplasms epithelial-mesenchymal transition migration
分类号:
R392.11;R737.9
DOI:
10.13362/j.qlyx.201703001
文献标志码:
A
摘要:
目的 探讨趋化因子CXC型趋化因子配体1(CXCL1)对人乳癌细胞MCF-7迁移能力和上皮-间质转化(EMT)的影响及其机制。
方法 体外培养人乳癌细胞MCF-7,分为对照组、CXCL1处理组、CXC趋化因子受体2(CXCR2)抑制剂组,应用CCK8方法检测各组细胞增殖活性,以ELISA法检测各组细胞E-cadherin、Vimentin、p-PI3K、p-AKT蛋白表达,RT-PCR方法检测E-cadherin、Vimentin mRNA表达。
结果 CCK8检测结果显示,与对照组比较,CXCL1处理组细胞增殖活性升高(F=58.89,q=8.96,P<0.01),CXCR2抑制剂组细胞增殖活性降低(q=6.31,P<0.05)。RT-PCR结果显示,与对照组相比较,CXCL1处理组E-cadherin mRNA表达下调(t=4.07,P<0.01),Vimentin mRNA表达上调(t=3.62,P<0.05)。ELISA检测结果显示,与对照组比较,CXCL1处理组E-cadherin蛋白表达下调(F=8.95,q=2.02,P<0.05),Vimentin蛋白表达上调(F=111.50,q=14.48,P<0.01),CXCR2抑制剂组E-cadherin表达上调(q=2.04,P<0.05),Vimentin蛋白表达下调(q=6.08,P<0.05);与对照组比较,CXCL1处理组PI3K、PAKT蛋白表达明显升高(F=60.35、28.15,q=10.52、5.37,P<0.01),CXCR2抑制剂组细胞内p-PI3K、p-AKT蛋白表达降低(q=4.65、4.97,P<0.05)。
结论 乳癌细胞可能通过CXCL1/CXCR2轴活化PI3K/AKT信号通路发生EMT。
Abstract:
Objective  To investigate the effects of chemokine (CXC motif) ligand 1 (CXCL1) on the migration and epithelial-mesenchymal transition (EMT) of human breast cancer cells (MCF-7) and its mechanism.
Methods  MCF-7 cells were cultured in vitro and divided into three groups: control group, CXCL1 (40 μg/L) group, and CXC chemokine receptor 2 (CXCR2) inhibitor (SB225002 10 mmol/L) group. Cell Counting Kit-8 (CCK8) was used to evaluate the proliferative activity of MCF-7 cells in all groups. Furthermore, enzyme-linked immunosorbent assay (ELISA) was used to measure the protein expression of E-cadherin, vimentin, p-PI3K, and p-AKT. The expression of E-cadherin mRNA and Vimentin mRNA was measured by RT-PCR.
Results  CCK8 assay results showed that compared with the control group, the CXCL1 group had a significantly higher cell proliferative activity (F=58.89,q=8.96,P<0.01), while the CXCR2 inhibitor group had a significantly lower cell proliferative activity (q=6.31,P<0.05). The RT-PCR results indicated that the CXCL1 group had significantly lower expression of E-cadherin mRNA and significantly higher expression of Vimentin mRNA than the control group (t=4.07,3.62;P<0.05). The ELISA results showed that the CXCL1 group had significantly lower protein expression of E-cadherin and significantly higher protein expression of Vimentin (F=8.95,q=2.02,P<0.05; F=111.50,q=14.48,P<0.01); while the CXCR2 inhibitor group had significantly higher protein expression of E-cadherin and significantly lower protein expression of Vimentin (q=2.04,6.08;P<0.05). The CXCL1 group had significantly higher protein expression of p-PI3K and p-AKT than the control group (F=60.35,q=10.52,P<0.01;F=28.15,q=5.37,P<0.01); the CXCR2 inhibitor group had significantly lower protein expression of p-PI3K and p-AKT than the control group (q=4.65,4.97;P<0.05).
Conclusion  Chemokine CXCL1 plays a key role in EMT of MCF-7 cells by activating the PI3K/AKT signaling pathway through CXCL1/CXCR2 axis.
更新日期/Last Update: 2017-08-12