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对于肝癌细胞系，无论有无9-顺式视黄酸或细胞毒性药物，曲格列酮在临床可达到的浓度下均无效。

Lack of efficacy of troglitazone at clinically achievable concentrations, with or without 9-cis retinoic acid or cytotoxic agents, for hepatocellular carcinoma cell lines.

作者信息

Shen Y-C, Hsu C, Chen J-Y, Cheng A-L

机构信息

Department of Oncology, National Taiwan University Hospital, Taipei, Taiwan.

出版信息

Br J Cancer. 2004 Oct 18;91(8):1561-5. doi: 10.1038/sj.bjc.6602200.

DOI:10.1038/sj.bjc.6602200
PMID:15467764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2409938/
Abstract

Although the PPARgamma agonist troglitazone has been shown to induce growth inhibition of hepatocellular carcinoma (HCC) cells at high concentration, this study indicates troglitazone does not significantly inhibit the growth of HCC cells at clinically achievable concentrations (1-10 microM), and this lack of activity could not be improved by the addition of 9-cis-retinoic acid. Furthermore, no synergistic effect was found between troglitazone and cytotoxic anticancer agents.

摘要

尽管已表明过氧化物酶体增殖物激活受体γ（PPARγ）激动剂曲格列酮在高浓度时可诱导肝癌（HCC）细胞生长抑制，但本研究表明，曲格列酮在临床可达到的浓度（1 - 10微摩尔）下并不会显著抑制HCC细胞的生长，并且添加9 - 顺式视黄酸也无法改善这种缺乏活性的情况。此外，未发现曲格列酮与细胞毒性抗癌药物之间存在协同作用。

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1
Lack of efficacy of troglitazone at clinically achievable concentrations, with or without 9-cis retinoic acid or cytotoxic agents, for hepatocellular carcinoma cell lines.对于肝癌细胞系，无论有无9-顺式视黄酸或细胞毒性药物，曲格列酮在临床可达到的浓度下均无效。
Br J Cancer. 2004 Oct 18;91(8):1561-5. doi: 10.1038/sj.bjc.6602200.
2
A ligand for peroxisome proliferator activated receptor gamma inhibits cell growth and induces apoptosis in human liver cancer cells.过氧化物酶体增殖物激活受体γ的一种配体可抑制人肝癌细胞的生长并诱导其凋亡。
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Peroxisome proliferator-activated receptor gamma ligand troglitazone induces cell cycle arrest and apoptosis of hepatocellular carcinoma cell lines.过氧化物酶体增殖物激活受体γ配体曲格列酮诱导肝癌细胞系的细胞周期停滞和凋亡。
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本文引用的文献

1
Peroxisome proliferator-activated receptor gamma and cancers.过氧化物酶体增殖物激活受体γ与癌症
Clin Cancer Res. 2003 Jan;9(1):1-9.
2
Peroxisome proliferator-activated receptor gamma ligand troglitazone induces cell cycle arrest and apoptosis of hepatocellular carcinoma cell lines.过氧化物酶体增殖物激活受体γ配体曲格列酮诱导肝癌细胞系的细胞周期停滞和凋亡。
Cancer. 2002 Nov 15;95(10):2243-51. doi: 10.1002/cncr.10906.
3
PPARgamma ligands inhibit primary tumor growth and metastasis by inhibiting angiogenesis.过氧化物酶体增殖物激活受体γ（PPARγ）配体通过抑制血管生成来抑制原发性肿瘤的生长和转移。
J Clin Invest. 2002 Oct;110(7):923-32. doi: 10.1172/JCI15634.
4
Basal levels and patterns of anticancer drug-induced activation of nuclear factor-kappaB (NF-kappaB), and its attenuation by tamoxifen, dexamethasone, and curcumin in carcinoma cells.癌细胞中抗癌药物诱导的核因子-κB（NF-κB）激活的基础水平和模式，以及他莫昔芬、地塞米松和姜黄素对其的抑制作用
Biochem Pharmacol. 2002 May 1;63(9):1709-16. doi: 10.1016/s0006-2952(02)00931-0.
5
Differentiating members of the thiazolidinedione class: a focus on efficacy.噻唑烷二酮类药物的差异：聚焦疗效
Diabetes Metab Res Rev. 2002 Mar-Apr;18 Suppl 2:S16-22. doi: 10.1002/dmrr.251.
6
Peroxisome proliferator-activated receptor gamma augments tumor necrosis factor family-induced apoptosis in hepatocellular carcinoma.过氧化物酶体增殖物激活受体γ增强肿瘤坏死因子家族诱导的肝细胞癌凋亡。
Anticancer Drugs. 2002 Jan;13(1):59-65. doi: 10.1097/00001813-200201000-00007.
7
Anticancer effects of thiazolidinediones are independent of peroxisome proliferator-activated receptor gamma and mediated by inhibition of translation initiation.噻唑烷二酮类药物的抗癌作用独立于过氧化物酶体增殖物激活受体γ，且由抑制翻译起始介导。
Cancer Res. 2001 Aug 15;61(16):6213-8.
8
Peroxisome proliferator-activated receptor gamma ligand-induced growth inhibition of human hepatocellular carcinoma.过氧化物酶体增殖物激活受体γ配体诱导的人肝癌细胞生长抑制
Br J Cancer. 2001 Jun 15;84(12):1640-7. doi: 10.1054/bjoc.2001.1821.
9
Peroxisome proliferator-activated receptor gamma and metabolic disease.过氧化物酶体增殖物激活受体γ与代谢性疾病
Annu Rev Biochem. 2001;70:341-67. doi: 10.1146/annurev.biochem.70.1.341.
10
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Hepatology. 2001 May;33(5):1087-97. doi: 10.1053/jhep.2001.24024.