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尼拉帕利增强神经节苷脂GD2的作用并与之协同,以增强其对膀胱癌细胞的抑制作用。

Niraparib Enhances and Synergizes with Ganglioside GD2 to Potentiate its Inhibitory Effect on Bladder Cancer Cells.

作者信息

Lu Shan, Gao Xiaojia, Li Xin, Zhao Hongchao, Lu Hongda

机构信息

Department of Oncology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430014, China.

Department of Hospital -Acquired Infection Control, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology.

出版信息

Comb Chem High Throughput Screen. 2024 Oct 1. doi: 10.2174/0113862073343602240909115320.

Abstract

PURPOSE

This study aimed to study the inhibitory effect of niraparib alone or in combination with GD2 specific antibody on Bladder Cancer (BCa).

METHODS

The migration ability of BCa cells was assessed through a scratch assay. CCK-8 assay was performed to evaluate the viability of BCa cells, and Transwell invasion assays were utilized to examine invasive capacity. The expression levels of E-cadherin and vimentin in BCa cells were measured using QRT-PCR.

RESULTS

Western blot showed the EMT level to be the lowest in the niraparib+GD2 group. The transwell invasion assay suggested that the invasion ability of BCa cells was weakened in the niraparib+ GD2 group. CCK8 assay indicated that the proliferation ability of BCa cells was decreased. Scratch test suggested that the migration ability of BCa cells was weakened. PCR result showed that the niraparib + GD2 group had the most significant inhibitory effect on mRNA expression of EMT markers.

CONCLUSION

Niraparib combined with a GD2-specific antibody exerted a more prominent inhibitory effect on BCa.

摘要

目的

本研究旨在探讨尼拉帕利单独或与GD2特异性抗体联合应用对膀胱癌(BCa)的抑制作用。

方法

通过划痕试验评估BCa细胞的迁移能力。采用CCK-8试验评估BCa细胞的活力,并利用Transwell侵袭试验检测侵袭能力。使用QRT-PCR检测BCa细胞中E-钙黏蛋白和波形蛋白的表达水平。

结果

蛋白质印迹法显示尼拉帕利+GD2组的上皮-间质转化(EMT)水平最低。Transwell侵袭试验表明,尼拉帕利+GD2组中BCa细胞的侵袭能力减弱。CCK8试验表明BCa细胞的增殖能力下降。划痕试验表明BCa细胞的迁移能力减弱。PCR结果显示,尼拉帕利+GD2组对EMT标志物的mRNA表达具有最显著的抑制作用。

结论

尼拉帕利联合GD2特异性抗体对BCa具有更显著的抑制作用。

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