首页|尼卡地平调节RhoA/ROCK信号通路对膀胱癌细胞增殖、凋亡和化疗耐药性的影响

尼卡地平调节RhoA/ROCK信号通路对膀胱癌细胞增殖、凋亡和化疗耐药性的影响

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该文旨在探讨尼卡地平基于RhoA/ROCK信号通路对膀胱癌细胞增殖、凋亡及化疗耐药性的影响.将膀胱癌细胞T24分为对照组、L-尼卡地平组、M-尼卡地平组、H-尼卡地平组、H-尼卡地平+LPA组、DMSO组、顺铂组、H-尼卡地平+顺铂组、H-尼卡地平+顺铂+LPA组.分别利用CCK-8试剂盒、流式细胞术、划痕实验、Transwell法、Western blot方法检测T24细胞的增殖活性、凋亡、迁移、侵袭能力以及RhoA/ROCK信号通路蛋白表达情况.与对照组比较,L-尼卡地平组、M-尼卡地平组、H-尼卡地平组细胞D值、划痕愈合率、侵袭细胞数、RhoA及ROCK蛋白表达水平显著降低(P<0.05),细胞凋亡率显著升高(P<0.05);与H-尼卡地平组比较,H-尼卡地平+LPA组细胞D值、划痕愈合率、侵袭细胞数、RhoA及ROCK蛋白表达水平显著升高(P<0.05),细胞凋亡率显著降低(P<0.05);与DMSO组比较,顺铂组细胞D值、划痕愈合率、侵袭细胞数均降低,凋亡率升高(P<0.05);与顺铂组比较,H-尼卡地平组和H-尼卡地平+顺铂组细胞D值、划痕愈合率、侵袭细胞数均降低,凋亡率升高(P<0.05);与H-尼卡地平+顺铂组比较,H-尼卡地平+顺铂+LPA组D值、划痕愈合率、侵袭细胞数均升高,凋亡率降低(P<0.05).尼卡地平可以抑制膀胱癌细胞增殖及其化疗耐药性,促进细胞凋亡,其作用机制可能与抑制RhoA/ROCK信号通路有关.
Effects of Nicardipine on Proliferation,Apoptosis and Chemoresistance of Bladder Cancer Cells by Regulating RhoA/ROCK Signaling Pathway
The aim of this study was to investigate the effect of nicardipine on the proliferation,apoptosis and chemoresistance of bladder cancer cells by regulating RhoA/ROCK signaling pathway.T24 cells of blad-der cancer were separated into control group,L-nicardipine group,M-nicardipine group,H-nicardipine group,H-nicardipine+LPA group,DMSO group,cisplatin group,H-nicardipine+cisplatin group,H-nicardipine+cisplatin group,and H-nicardipine+cisplatin+LPA group.The proliferation activity,apoptosis,migration,invasion ability,and RhoA/ROCK signaling pathway protein expression of T24 cells were detected using CCK-8 assay kit,flow cytometry,scratch assay,Transwell method,and Western blot,respectively.Compared with the control group,the D value,scratch healing rate,number of invasive cells,and the RhoA and ROCK protein expression levels in the L-nicardipine group,M-nicardipine group,and H-nicardipine group were obviously reduced(P<0.05),while the apoptosis rate of cells was obviously increased(P<0.05).Compared with the H-nicardipine group,the D value,scratch healing rate,number of invasive cells,and the RhoA and ROCK expression levels in H-nicardipine+LPA group were obviously increased(P<0.05),while the apoptosis rate of cells was obviously decreased(P<0.05).Compared with the DMSO group,the D value,scratch healing rate,and number of invasive cells in the cisplatin group were decreased,while the apoptosis rate was increased(P<0.05).Compared with the cisplatin group,the D value,scratch healing rate,and number of invasive cells in the H-nicardipine group and the H-nicardipine+cisplatin group were decreased,while the apoptosis rate was increased(P<0.05).Compared with the H-nicardipine+cisplatin group,the H-nicardipine+cisplatin+LPA group showed an increase in D value,scratch healing rate,and number of invasive cells,and a decrease in apoptosis rate(P<0.05).Nicardipine can inhibit the proliferation and chemoresis-tance of bladder cancer cells,and promote cell apoptosis.The mechanism may be related to the inhibition of RhoA/ROCK signaling pathway.

nicardipineRhoA/ROCK signaling pathwaybladder cancerproliferationapoptosischemo-resistance

庞允、杨京可、李荣芳、杨浩杰、李利利、白婷婷

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西安交通大学医院药剂科,西安 710049

西安市第九医院泌尿外科,西安 710054

西安市第九医院心血管病院三科,西安 710054

西安交通大学医院公卫中心,西安 710049

西安交通大学医院体检中心,西安 710049

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尼卡地平 RhoA/ROCK信号通路 膀胱癌 增殖 凋亡 化疗耐药性

2024

中国细胞生物学学报
中国科学院上海生命科学研究院,生物化学与细胞生物学研究所,中国细胞生物学学会

中国细胞生物学学报

CSTPCD
影响因子:0.554
ISSN:1674-7666
年,卷(期):2024.46(6)
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