Isosilybin B and isosilybin A inhibit growth, induce G<sub>1</sub> arrest and cause apoptosis in human prostate cancer LNCaP and 22Rv1 cells

Gagan Deep1 Nicholas H. Oberlies2 David J. Kroll2 and Rajesh Agarwal13

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Isosilybin B and isosilybin A inhibit growth, induce G₁ arrest and cause apoptosis in human prostate cancer LNCaP and 22Rv1 cells

机译：异水飞蓟宾B和异水飞蓟宾A抑制人前列腺癌LNCaP和22Rv1细胞的生长，诱导G _{1 阻滞并引起细胞凋亡}

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Silymarin and, one of its constituents, silibinin exert strong efficacy against prostate cancer (PCA); however, anticancer efficacy and associated mechanisms of other components of silymarin, which is a mixture of flavonolignans, are largely unknown. Here we have assessed the anticancer efficacy of two pure compounds isosilybin B and isosilybin A, isolated from silymarin, in human prostate carcinoma LNCaP and 22Rv1 cells. Isosilybin B and isosilybin A treatment resulted in growth inhibition and cell death together with a strong G₁ arrest and apoptosis in both the cell lines. In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level. Isosilybin B- and isosilybin A-induced apoptosis was accompanied with an increase in the cleavage of poly (ADP-ribose) polymerase, caspase-9 and caspase-3 and a decrease in survivin levels. Compared with LNCaP and 22Rv1 cells, the antiproliferative and cytotoxic potentials of isosilybin B and isosilybin A were of much lesser magnitude in non-neoplastic human prostate epithelial PWR-1E cells suggesting the transformation-selective effect of these compounds. Together, this study for the first time identified that isosilybin B and isosilybin A, two diastereoisomers isolated from silymarin, have anti-PCA activity that is mediated via cell cycle arrest and apoptosis induction.

机译：水飞蓟素及其成分之一水飞蓟宾对前列腺癌（PCA）具有强大的功效；然而，水飞蓟素（黄酮木聚糖的混合物）的其他成分的抗癌功效和相关机制在很大程度上尚不清楚。在这里，我们评估了从水飞蓟素中分离得到的两种纯化合物异水飞蓟宾B和异水飞蓟宾A在人前列腺癌LNCaP和22Rv1细胞中的抗癌作用。异水飞蓟宾B和异水飞蓟宾A处理导致生长抑制和细胞死亡，以及两个细胞系中强烈的G _{1 阻滞和凋亡。在研究细胞周期和凋亡调节剂变化的研究中，异水飞蓟宾B和异水飞蓟宾A导致细胞周期蛋白（D1，D3，E和A）和细胞周期蛋白依赖性激酶（Cdk2，Cdk4和细胞分裂周期25A）的水平降低），但会导致p21，p27和p53的水平增加，但在22Rv1细胞中，异麦冬蛋白B导致p21蛋白质的水平下降。异水飞蓟宾B和异水飞蓟宾A诱导的细胞凋亡伴随着多聚（ADP-核糖）聚合酶，caspase-9和caspase-3的切割增加以及生存素水平降低。与LNCaP和22Rv1细胞相比，异水飞蓟宾B和异水飞蓟宾A在非肿瘤性人前列腺上皮PWR-1E细胞中的抗增殖和细胞毒性潜力要小得多，表明这些化合物的转化选择性作用。总之，这项研究首次确定了从水飞蓟素分离出的两种非对映异构体异水飞蓟宾B和异水飞蓟宾A具有抗PCA活性，该活性是通过细胞周期停滞和凋亡诱导介导的。}

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《Carcinogenesis》 |2007年第7期|1533-1542|共10页
作者
Gagan Deep1 Nicholas H. Oberlies2 David J. Kroll2 and Rajesh Agarwal13;
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Department of Pharmaceutical Sciences School of Pharmacy University of Colorado Health Sciences Center Denver CO USA;

Natural Products Laboratory Center for Organic and Medicinal Chemistry Research Triangle Institute Research Triangle Park NC USA;

University of Colorado Cancer Center University of Colorado Health Sciences Center Denver CO USA;

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1. Proteasome inhibitor PS-341 down-regulates prostate-specific antigen (PSA) and induces growth arrest and apoptosis of androgen-dependent human prostate cancer LNCaP cells. [J] . Ikezoe T, Yang Y, Saito T, Cancer science. . 2004,第3期

机译：蛋白酶体抑制剂PS-341下调前列腺特异性抗原（PSA），并诱导雄激素依赖性人前列腺癌LNCaP细胞生长停滞和凋亡。
2. Isosilybin A induces apoptosis in human prostate cancer cells via targeting Akt, NF-kappaB, and androgen receptor signaling. [J] . Deep G, Gangar SC, Oberlies NH, Molecular Carcinogenesis . 2010,第10期

机译：异水飞蓟宾A通过靶向Akt，NF-κB和雄激素受体信号传导诱导人前列腺癌细胞凋亡。
3. HIV-1 protease inhibitor induces growth arrest and apoptosis of human prostate cancer LNCaP cells in vitro and in vivo in conjunction with blockade of androgen receptor STAT3 and AKT signaling. [J] . Yang Y, Ikezoe T, Takeuchi T, Cancer science. . 2005,第7期

机译：HIV-1蛋白酶抑制剂与雄激素受体STAT3和AKT信号传导阻滞一起，在体外和体内诱导人前列腺癌LNCaP细胞的生长停滞和凋亡。
4. Silencing of the Fatty Acid Synthase Gene by RNA Interference Inhibits Growth and Induces Apoptosis of LNCaP Prostate Cancer Cells [C] . Ellen De Schrijver, Koen Brusselmans, Walter Heyns, International Symposium on Hormonal Carcinogenesis . 2005

机译：通过RNA干扰沉默脂肪酸合成酶基因抑制生长并诱导LNCAP前列腺癌细胞的凋亡
5. Multiple Akt/PKB-independent survival signaling pathways inhibit apoptosis in LNCaP prostate cancer cells. [D] . Carson, Jonathan Paul. 2002

机译：多个独立于Akt / PKB的生存信号通路抑制LNCaP前列腺癌细胞的凋亡。
6. Isosilybin A Induces Apoptosis in Human Prostate Cancer Cells via Targeting Akt NF-κB and Androgen Receptor Signaling [O] . Gagan Deep, Subhash Chander Gangar, Nicholas H. Oberlies, -1

机译：isosilyb a通过靶向aktnf-κb和雄激素受体信号传导诱导人前列腺癌细胞中的细胞凋亡
7. Isosilybin B and isosilybin A inhibit growth, induce G1 arrest and cause apoptosis in human prostate cancer LNCaP and 22Rv1 cells [O] . Gagan Deep, Nicholas H. Oberlies, David J. Kroll, 2007

机译：IsoSiLybin B和IsoSiLyb抑制生长，诱导G1抑制和引起人前列腺癌LNCAP和22rv1细胞的细胞凋亡

Isosilybin B and isosilybin A inhibit growth, induce G1 arrest and cause apoptosis in human prostate cancer LNCaP and 22Rv1 cells

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Isosilybin B and isosilybin A inhibit growth, induce G₁ arrest and cause apoptosis in human prostate cancer LNCaP and 22Rv1 cells