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| 1 | 川陈皮素对人前列腺癌DU145细胞生长的抑制作用及其机制显示文摘目的:检测川陈皮素对人前列腺癌DU145细胞增殖、凋亡、迁移和侵袭能力的影响,探讨其作用机制。方法:将培养的人前列腺癌DU145细胞分为对照组和0.8、1.6、3.2、6.4、12.8、25.6和51.2μmol·L^-1川陈皮素组。MTT法检测各组人前列腺癌DU145细胞的增殖活性,细胞划痕实验分析各组人前列腺癌DU145细胞迁移能力,Transwell实验分析各组人前列腺癌DU145细胞侵袭能力,流式细胞术检测各组人前列腺癌DU145细胞凋亡率,Western blotting法检测各组人前列腺癌DU145细胞中磷酸化c-Jun氨基末端激酶(p-JNK)、磷酸化P38丝裂原活化蛋白酶(p-P38)和磷酸化细胞外调节蛋白激酶(p-ERK)蛋白表达水平。结果:与对照组比较,作用24、48和72 h时,25.6μmol·L^-1川陈皮素组人前列腺癌DU145细胞增殖活性明显降低(P<0.01),川陈皮素对DU145细胞的增殖抑制作用呈现时间和浓度依赖性。与对照组比较,作用48 h后,12.8μmol·L^-1川陈皮素组人前列腺癌DU145细胞划痕愈合率和侵袭细胞数明显降低(P<0.01),人前列腺癌DU145细胞中p-ERK蛋白表达水平降低(P<0.01);25.6μmol·L^-1川陈皮素组人前列腺癌DU145细胞中p-ERK蛋白表达水平降低(P<0.01),但细胞凋亡率明显升高(P<0.01),p-JNK和p-P38蛋白表达水平升高(P<0.01)。结论:川陈皮素对人前列腺癌DU145细胞生长具有抑制作用,可促进细胞凋亡,抑制细胞增殖、迁移和侵袭;MAPK途径相关蛋白表达的改变可能是川陈皮素对DU145细胞生长抑制作用的机制之一。 | 张阳 姜华茂 | 2020 | 吉林大学学报(医学版)2020，46，6： | 12 |
| 2 | Oxidative stress and redox signaling in CRPC progression: therapeutic potential of clinically-tested Nrf2-activators显示文摘Androgen deprivation therapy(ADT)is the mainstay regimen in patients with androgen-dependent prostate cancer(PCa).However,the selection of androgen-independent cancer cells leads to castrate resistant prostate cancer(CRPC).The aggressive phenotype of CRPC cells underscores the need to elucidate mechanisms and therapeutic strategies to suppress CRPC outgrowth.Despite ADT,the activation of androgen receptor(AR)transcription factor continues via crosstalk with parallel signaling pathways.Understanding of how these signaling cascades are initiated and amplified post-ADT is lacking.Hormone deprivation can increase oxidative stress and the resultant reactive oxygen species(ROS)may activate both AR and non-AR signaling.Moreover,ROS-induced inflammatory cytokines may further amplify these redox signaling pathways to augment AR function.However,clinical trials using ROS quenching small molecule antioxidants have not suppressed CRPC progression,suggesting that more potent and persistent suppression of redox signaling in CRPC cells will be needed.The transcription factor Nrf2 increases the expression of numerous antioxidant enzymes and downregulates the function of inflammatory transcription factors,e.g.,nuclear factor kappa B.We documented that Nrf2 overexpression can suppress AR-mediated transcription in CRPC cell lines.Furthermore,two Nrf2 activating agents,sulforaphane(a phytochemical)and bardoxolone-methyl(a drug in clinical trial)suppress AR levels and sensitize CRPC cells to anti-androgens.These observations implicate the benefits of potent Nrf2-activators to suppress the lethal signaling cascades that lead to CRPC outgrowth.This review article will address the redox signaling networks that augment AR signaling during PCa progression to CRPC,and the possible utility of Nrf2-activating agents as an adjunct to ADT. | Debasis Mondal Devin Narwani Shahnawaz Notta Dawood Ghaffar Nikhil Mardhekar Syed S.A.Quadri | 2021 | Cancer Drug Resistance2021，4，1： | 1 |
| 3 | 雷公藤红素对前列腺癌DU-145细胞生物学行为的影响及机制研究显示文摘目的探讨雷公藤红素对前列腺癌DU-145细胞生物学行为的影响及可能机制。方法体外培养DU-145细胞,分别以2.5、5.0、10.0μmol/L雷公藤红素处理,对照组细胞以等量0.9%NaCl处理。给药48 h后,MTT实验与平板克隆实验检测DU-145细胞增殖能力;Transwell实验检测DU-145细胞迁移和侵袭能力;流式细胞术检测DU-145细胞的凋亡;Western blot检测细胞周期蛋白Dl(cyclin D1)、血管内皮生长因子(vascular endothelial growth factor,VEGF)和基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)的蛋白表达水平。结果不同浓度雷公藤红素处理后,DU-145细胞的细胞活力降低、迁移和侵袭能力降低,细胞凋亡率明显升高,DU-145细胞cyclin D1、VEGF与MMP-9的表达水平均明显降低(P<0.01)。结论雷公藤红素抑制人前列腺癌DU-145细胞增殖、侵袭及迁移,促进凋亡。 | 孙强 王科峰 费翔 齐漫龙 | 2021 | 解剖科学进展2021，27，2： | 0 |
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