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STAT3基因联合顺铂对人肾母细胞瘤SK-NEP-1细胞生长的抑制作用。

Inhibitory effect of STAT3 gene combined with CDDP on growth of human Wilms tumour SK-NEP-1 cells.

作者信息

Wang Junrong, Zhang Nina, Qu Haijiang, You Guangxian, Yuan Junhui, Chen Caie, Li Wenyi, Pan Feng

机构信息

Department of Laboratory Medicine, Wenling Maternal and Child Health Care Hospital, Wenling 317500, Zhejiang Province, China.

Department of Oncology, The Second People's Hospital of Wenling City (Cancer Hospital in Taizhou, Shanghai Tumor Hospital in Taizhou Branch), Wenling 317502, Zhejiang Province, China.

出版信息

Biosci Rep. 2016 Jun 3;36(3). doi: 10.1042/BSR20160072. Print 2016 Jul.

DOI:10.1042/BSR20160072
PMID:27129294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5293582/
Abstract

To investigate the effects of signal transducer and activator of transcription 3 (STAT3) combined with cisplatin (CDDP) on the growth of human Wilms tumour (WT) SK-NEP-1 cell subcutaneous xenografts in nude mice and the possible mechanisms. Human WT SK-NEP-1 cells were subcutaneously transplanted to establish the BALB/c nude mice xenograft model. Mice were randomly divided into five groups: blank control group, adenovirus control group (NC group), STAT3 group, CDDP group and STAT3 plus CDDP group (combination group). Tumour volume and tumour weight were observed during the therapeutic process. The expression levels of STAT3, glucose regulatory protein 78 (GRP78) and BCL2-associated X protein (BAX) were evaluated by immunohistochemical analysis. Compared with the STAT3 group or CDDP group, the tumour weight and volume was significantly reduced in the combination group (P<0.05). No statistical significance was found in NC group compared with the blank control group (P > 0.05). Immunohistochemical analysis showed that STAT3, GRP78 and BAX protein levels in the combination group were significantly higher than those in STAT3 group and CDDP group (P<0.05). Exogenous STAT3 and CDDP may synergistically inhibit the xenograft tumour growth through up-regulation of BAX protein via GRP78.

摘要

探讨信号转导与转录激活因子3(STAT3)联合顺铂(CDDP)对人肾母细胞瘤(WT)SK-NEP-1细胞皮下异种移植瘤在裸鼠体内生长的影响及可能机制。将人WT SK-NEP-1细胞皮下移植建立BALB/c裸鼠异种移植瘤模型。小鼠随机分为五组:空白对照组、腺病毒对照组(NC组)、STAT3组、CDDP组和STAT3加CDDP组(联合组)。在治疗过程中观察肿瘤体积和肿瘤重量。通过免疫组织化学分析评估STAT3、葡萄糖调节蛋白78(GRP78)和BCL2相关X蛋白(BAX)的表达水平。与STAT3组或CDDP组相比,联合组的肿瘤重量和体积显著降低(P<0.05)。NC组与空白对照组相比无统计学意义(P>0.05)。免疫组织化学分析显示,联合组中STAT3、GRP78和BAX蛋白水平显著高于STAT3组和CDDP组(P<0.05)。外源性STAT3和CDDP可能通过GRP78上调BAX蛋白协同抑制异种移植瘤生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/70e381b03343/bsr036e342fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/d2f36231a4d9/bsr036e342fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/75c42f8782c0/bsr036e342fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/70e381b03343/bsr036e342fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/d2f36231a4d9/bsr036e342fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/75c42f8782c0/bsr036e342fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbeb/5293582/70e381b03343/bsr036e342fig3.jpg

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本文引用的文献

1
Intraoperative tumor lysis syndrome in a child with Wilms' tumor.一名患肾母细胞瘤儿童的术中肿瘤溶解综合征
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Oncotarget. 2015 Dec 29;6(42):44675-87. doi: 10.18632/oncotarget.5971.
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STAT3 selectively interacts with Smad3 to antagonize TGF-β signalling.信号转导及转录激活因子3(STAT3)与Smad3特异性相互作用,以拮抗转化生长因子-β(TGF-β)信号传导。
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Homoharringtonine induces apoptosis and inhibits STAT3 via IL-6/JAK1/STAT3 signal pathway in Gefitinib-resistant lung cancer cells.高三尖杉酯碱通过IL-6/JAK1/STAT3信号通路诱导吉非替尼耐药肺癌细胞凋亡并抑制STAT3。
Sci Rep. 2015 Jul 13;5:8477. doi: 10.1038/srep08477.
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Elatoside C protects against hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes through the reduction of endoplasmic reticulum stress partially depending on STAT3 activation.刺囊酸C通过部分依赖于信号转导和转录激活因子3(STAT3)激活来减轻内质网应激,从而保护H9c2心肌细胞免受缺氧/复氧诱导的细胞凋亡。
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