首页|CX3CL1促进三阴性乳腺癌细胞株多柔比星/紫杉醇化疗的耐药机制观察

CX3CL1促进三阴性乳腺癌细胞株多柔比星/紫杉醇化疗的耐药机制观察

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目的 探究 CX3CL1 基因对于三阴性乳腺癌对多柔比星和紫杉醇化疗药物耐药性的促进机制.方法 通过CX3CL1 基因过表达慢病毒载体构建、Western Blot检测乳腺癌细胞中CX3CL1 的表达、Q-PCR检测细胞中基因表达、CCK-8 实验检测细胞活力、EdU检测细胞增殖、Annexin V-FITC/PI染色流式细胞术检测细胞凋亡、Transwell检测细胞迁移率、Elisa试剂盒检测细胞内和培养上清液中CX3CL1 表达、应用SPSS 19.0 统计学软件,应用Pearson卡方检验分析三阴性乳腺癌中CX3CL1 的表达.累计生存率的计算采用Kaplan-Meier方法.结果 构建的CX3CL1 过表达慢病毒感染MDA-MB-231细胞载体结果发现CX3CL1 具有促进细胞活力、促进细胞增殖、抑制细胞凋亡、促进细胞迁移等作用.通过人单核白血病细胞结合发现CX3CL1 具有诱导巨噬细胞向M2 型极化,促进细胞迁移的作用.结论 CX3CL1 通过促进巨噬细胞向M2 型极化,抑制细胞凋亡以及促进细胞迁移来降低乳腺癌细胞对多柔比星/紫杉醇化疗药物的敏感性从而导致耐药性产生的机制.
Mechanism Observation of CX3CL1 Promoting Doxorubicin/Paclitaxel Chemoresistance in Triple Negative Breast Cancer
Objective To explore the mechanism of CX3CL1 gene promoting drug resistance to doxorubicin and paclitaxel in tri-ple negative breast cancer.Methods CX3CL1 gene overexpression lentiviral vector was constructed,CX3CL1 expression in breast cancer cells was detected by Western Blot,gene expression in cells was detected by Q-PCR,cell viability was detected by CCK-8 as-say,Edu was used to detect cell proliferation,apoptosis was detected by flow cytometry with Annexin V-FITC/PI staining,Transwell was used to detect cell mobility,and CX3CL1 expression in intracellular and culture supernatant was detected by Elisa kit.The ex-pression of CX3CLI in triple-negative breast cancer was analyzed by SPSS 19.0 statistical software and Pearson Chi-square test.The cumulative survival rate was calculated by Kaplan-Meier method.Results The constructed CX3CL1 overexpression lentivirus infected MDA-MB-231 cell vector showed that CX3CL1 has the effects of promoting cell viability,promoting cell proliferation,inhibiting cell apoptosis,and promoting cell migration.Through the binding of human monocytic leukemia cells,it was found that CX3CL1 can in-duce macrophage polarization towards M2 type and promote cell migration.Conclusion CX3CL1 can reduce the sensitivity of breast cancer cells to doxorubicin/paclitaxel chemotherapy drugs by promoting the polarization of macrophages to M2 type,inhibiting cell ap-optosis and promoting cell migration,thus leading to the mechanism of drug resistance.

CX3CL1triple negative breast cancerchemotherapy drugsdrug resistance mechanism

张佳怡、陶维

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锦州医科大学附属第一医院,辽宁 锦州 121000

CX3CL1 三阴性乳腺癌 化疗药物 耐药机制

辽宁省科技厅计划项目

2023-MSLH-058

2024

锦州医科大学学报
辽宁医学院

锦州医科大学学报

影响因子:0.802
ISSN:1674-0424
年,卷(期):2024.45(4)