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Glucagon-like peptide-1 promotes islet cell growth and inhibits apoptosis in Zucker diabetic rats.胰高血糖素样肽-1促进Zucker糖尿病大鼠胰岛细胞生长并抑制其凋亡。
Endocrinology. 2002 Nov;143(11):4397-408. doi: 10.1210/en.2002-220405.
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A novel protein overexpressed in hepatoma accelerates export of NF-kappa B from the nucleus and inhibits p53-dependent apoptosis.一种在肝癌中过表达的新型蛋白质可加速核因子-κB从细胞核的输出，并抑制p53依赖性细胞凋亡。
Cancer Cell. 2002 Oct;2(4):335-46. doi: 10.1016/s1535-6108(02)00152-6.
3
Leptin and high glucose stimulate cell proliferation in MCF-7 human breast cancer cells: reciprocal involvement of PKC-alpha and PPAR expression.瘦素和高糖刺激MCF-7人乳腺癌细胞的细胞增殖：蛋白激酶C-α和过氧化物酶体增殖物激活受体表达的相互作用
Biochim Biophys Acta. 2002 Oct 21;1592(2):107-16. doi: 10.1016/s0167-4889(02)00276-8.
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Expression of p53 and C-myc genes and its clinical relevance in the hepatocellular carcinomatous and pericarcinomatous tissues.p53和C-myc基因在肝癌及癌旁组织中的表达及其临床意义
World J Gastroenterol. 2002 Oct;8(5):822-6. doi: 10.3748/wjg.v8.i5.822.
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Decreased peroxisome proliferator-activated receptor gamma gene expression is correlated with poor prognosis in patients with esophageal cancer.过氧化物酶体增殖物激活受体γ基因表达降低与食管癌患者的不良预后相关。
Jpn J Clin Oncol. 2002 Jul;32(7):238-43. doi: 10.1093/jjco/hyf056.
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Life Sci. 2002 Apr 19;70(22):2631-46. doi: 10.1016/s0024-3205(02)01510-2.
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Signal cross-talk between estrogen receptor alpha and beta and the peroxisome proliferator-activated receptor gamma1 in MDA-MB-231 and MCF-7 breast cancer cells.雌激素受体α和β与过氧化物酶体增殖物激活受体γ1在MDA-MB-231和MCF-7乳腺癌细胞中的信号串扰
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Androgen modulation of adhesion and antiadhesion molecules in PC-3 prostate cancer cells expressing androgen receptor.雄激素对表达雄激素受体的PC-3前列腺癌细胞中黏附分子和抗黏附分子的调节作用。
Endocrinology. 2002 Oct;143(10):3897-904. doi: 10.1210/en.2002-220156.
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Selective estrogen receptor (ER) modulators differentially regulate phospholipase D catalytic activity in ER-negative breast cancer cells.选择性雌激素受体（ER）调节剂对雌激素受体阴性乳腺癌细胞中的磷脂酶D催化活性有不同的调节作用。
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Experimental studies on the effects of the combined use of N-(4-hydroxyphenyl)retinamide (4-HPR) and tamoxifen (TAM) for estrogen receptor (ER)-negative breast cancer.N-(4-羟基苯基)视黄酸（4-HPR）与他莫昔芬（TAM）联合应用对雌激素受体（ER）阴性乳腺癌影响的实验研究
Kurume Med J. 2002;49(1-2):27-33. doi: 10.2739/kurumemedj.49.27.

过氧化物酶体增殖物激活受体γ配体抑制人肝癌BEL - 7402细胞的生长并诱导其凋亡。

Peroxisome proliferator-activated receptor gamma ligands inhibit cell growth and induce apoptosis in human liver cancer BEL-7402 cells.

作者信息

Li Ming-Yi, Deng Hua, Zhao Jia-Ming, Dai Dong, Tan Xiao-Yu

机构信息

Department of General Surgery, Affiliated Hospital of Guangdong Medical College, Zhangjiang 524001, Guangdong Province, China.

出版信息

World J Gastroenterol. 2003 Aug;9(8):1683-8. doi: 10.3748/wjg.v9.i8.1683.

DOI:10.3748/wjg.v9.i8.1683
PMID:12918101
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4611524/
Abstract

AIM

To investigate the characteristics of PPAR gamma ligands induced apoptosis in liver cancer cells.

METHODS

The effects of ligands for each of the PPAR gamma ligands on DNA synthesis and cell viability were examined in BEL-7402 liver cancer cells. Apoptosis was characterized by Hochest33258 staining, DNA fragmentation, TUNEL and ELISA, and cell cycle kinetics by FACS. Modulation of apoptosis related caspases expression by PPAR gamma ligands was examined by Western blot.

RESULTS

PPARgamma ligands, 15-deoxy-(12), (14)-prostaglandin J2 (15d-PGJ2) and troglitazone (TGZ), suppressed DNA synthesis of BEL-7402 cells. Both 15d-PGJ2 and TGZ induced BEL-7402 cell death in a dose dependent manner, which was associated with an increase in fragmented DNA and TUNEL-positive cells. At concentrations of 10 and 30 microM, 15d-PGJ(2) or troglitazone increased the proportion of cells with G(0)/G(1) phase DNA content and decreased those with S phase DNA content. There was no significant change in the proportion of cells with G(2)/M DNA content. The activities of Caspases-3, -6, -7 and -9 were increased by 15d-PGJ2 and TGZ treatment, while the activity of Caspase 8 had not significantly changed.

CONCLUSION

The present results suggest the potential usefulness of PPAR gamma ligands for chemoprevention and treatment of liver cancers.

摘要

目的

研究过氧化物酶体增殖物激活受体γ（PPARγ）配体诱导肝癌细胞凋亡的特性。

方法

检测了各PPARγ配体对BEL - 7402肝癌细胞DNA合成及细胞活力的影响。采用Hochest33258染色、DNA片段化分析、TUNEL法及酶联免疫吸附测定（ELISA）对细胞凋亡进行鉴定，通过流式细胞术（FACS）分析细胞周期动力学。采用蛋白质免疫印迹法检测PPARγ配体对凋亡相关半胱天冬酶表达的调节作用。

结果

PPARγ配体15 - 脱氧 - （12），（14）-前列腺素J2（15d - PGJ2）和曲格列酮（TGZ）抑制了BEL - 7402细胞的DNA合成。15d - PGJ2和TGZ均以剂量依赖性方式诱导BEL - 7402细胞死亡，这与DNA片段化增加及TUNEL阳性细胞增多有关。在10和30微摩尔浓度下，15d - PGJ2或曲格列酮增加了G0/G1期DNA含量细胞的比例，降低了S期DNA含量细胞的比例。G2/M期DNA含量细胞的比例无显著变化。15d - PGJ2和TGZ处理可增加半胱天冬酶 - 3、 - 6、 - 7和 - 9的活性，而半胱天冬酶8的活性无显著变化。

结论

目前的结果表明PPARγ配体在肝癌化学预防和治疗方面具有潜在的应用价值。