| 苏静,许芳,胡宏,文菁菁.TNFR2通过Akt和Wnt/β-4-4atenin信号途径对L428淋巴瘤细胞增殖和耐药的影响.[J].中南医学科学杂志.,2022,(1):51-54, 70. |
| TNFR2通过Akt和Wnt/β-4-4atenin信号途径对L428淋巴瘤细胞增殖和耐药的影响 |
| Effects of TNFR2 promoted cell proliferation and drug resistance of L428 lymphoma cells through Akt and Wnt /β-4-4catenin signaling pathway |
| 投稿时间:2021-03-06 修订日期:2021-09-30 |
| DOI:10.15972/j.cnki.43-1509/r.2022.01.011 |
| 中文关键词: L428淋巴瘤细胞 肿瘤坏死因子受体2 细胞增殖 耐药 蛋白激酶B Wnt/β-4-4atenin |
| 英文关键词:lymphoma L428 tumor necrosis factor receptor 2 cell proliferation drug resistance protein kinase B Wnt/β-4-4atenin |
| 基金项目:四川省科技计划项目(2014JY0019) 作者简介:苏静,硕士,主治医师,研究方向为淋巴瘤的诊断和治疗,E-mail为su97619172@163.com。 |
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| 中文摘要: |
| 目的探讨肿瘤坏死因子受体2(TNFR2)通过蛋白质丝氨酸苏氨酸激酶(Akt)和Wnt/β-4-4atenin信号途径对L428淋巴瘤细胞增殖和耐药的影响。方法L428细胞分为对照组、转染PcDNA3.1/TNFR2的上调组(UR组)、上调TNFR2并抑制Akt组(LY组)和上调TNFR2并抑制WNT通路组(DK组)。qRT-PCR检测各组TNFR2 mRNA表达,Western blot法检测TNFR2、磷酸化Akt(p-Akt)、Akt、β-4-4catenin蛋白表达,CCK-8法检测各组L428细胞增殖活性,分析阿霉素处理后IC50。过表达TNFR2后,采用TNFR2靶向拮抗剂处理,分别检测p-Akt、Akt、β-4-4catenin蛋白表达和细胞增殖率。结果UR组、LY组和DK组TNFR2 mRNA和蛋白表达、p-Akt/Akt、β-4-4catenin均高于对照组,LY组p-Akt/Akt低于UR组,DK组β-4-4catenin低于UR组(P<0.05)。UR组、LY组、DK组细胞活力OD值均高于对照组,UR组高于LY组和DK组(P<0.05)。UR、LY和DK组IC50高于对照组,LY和DK组IC50低于UR组(P<0.05)。TNFR2拮抗剂处理后p-Akt/Akt和β-4-4catenin表达均降低,且L428增殖率明显下降(P<0.05)。结论TNFR2通过Akt和WNT/β-4-4catenin途径促进淋巴瘤细胞L428增殖和ADM耐药,TNFR2可能是淋巴瘤治疗的新靶点。 |
| 英文摘要: |
| To investigate the effects of tumor necrosis factor receptor 2 (TNFR2) promoted cell proliferation and drug resistance of L428 lymphoma cells through protein serine threonine kinase (Akt) and Wnt /β-4-4catenin signaling pathway. MethodsL428 lymphoma cells were divided into four groups:control group (Group C) transfected with blank plasmid, upregulation group (Group UR) transfected with pcdna3.1/tnfr2, Upregulation of TNFR2 and inhibition of Akt group(Group LY) and Upregulation of TNFR2 and inhibition of Wnt pathway group(Group DK). qRT-PCR was used to detect the relative expression of TNFR2 mRNA. qRT-PCR was used to detect the relative expression of TNFR2 mRNA, and Western blot was used to detect the relative expression of TNFR2, p-Akt, Akt and β-4-4catenin protein.CCK-8 was used to detect the activity of L428 cells, and the IC50 of adriamycin treated cells was analyzed. After the overexpression of TNFR2, the relative expression levels of p-Akt, Akt and β-4-4catenin proteins were detected and the cell proliferation rate was detected by treating with TNFR2 targeted antagonist. ResultsThe expression of TNFR2 mRNA and protein, p-Akt/Akt and β-4-4catenin in UR, LY and DK groups were higher than those in control group, p-Akt/Akt in LY group was lower than that in UR group, β-4-4catenin in DK group was lower than that in UR group (P<0.05). The OD value of cell viability in UR group, LY group and DK group was higher than that in control group, and the OD value in UR group was higher than that in LY group and DK group (P<0.05). The IC50 in UR, LY and DK groups was higher than that in control group, and the IC50 in LY and DK groups was lower than that in UR group (P<0.05). After TNFR2 antagonist treatment, the expression of p-Akt/Akt and β-4-4catenin decreased, and the proliferation rate of L428 decreased significantly (P<0.05). ConclusionTNFR2 promotes the proliferation and ADM resistance of lymphoma l428 cells through Akt and Wnt/β-4-4catenin pathways, and TNFR2 may be a new target for the treatment of lymphoma. |
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