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本文引用的文献

1
Aberrant glycogen synthase kinase 3β is involved in pancreatic cancer cell invasion and resistance to therapy.异常的糖原合酶激酶 3β 参与胰腺癌细胞的侵袭和对治疗的耐药性。
PLoS One. 2013;8(2):e55289. doi: 10.1371/journal.pone.0055289. Epub 2013 Feb 8.
2
Targeting the hepatocyte growth factor-cMET axis in cancer therapy.针对癌症治疗中的肝细胞生长因子-cMET 轴。
J Clin Oncol. 2012 Sep 10;30(26):3287-96. doi: 10.1200/JCO.2011.40.3774. Epub 2012 Aug 6.
3
Glycogen synthase kinase-3 inhibition sensitizes pancreatic cancer cells to TRAIL-induced apoptosis.糖原合酶激酶-3 抑制使胰腺癌细胞对 TRAIL 诱导的细胞凋亡敏感。
PLoS One. 2012;7(7):e41102. doi: 10.1371/journal.pone.0041102. Epub 2012 Jul 19.
4
GSK-3β: A Bifunctional Role in Cell Death Pathways.糖原合成酶激酶-3β:在细胞死亡途径中的双重作用
Int J Cell Biol. 2012;2012:930710. doi: 10.1155/2012/930710. Epub 2012 May 21.
5
The Fbw7 and betaTRCP E3 ubiquitin ligases and their roles in tumorigenesis.Fbw7 和 betaTRCP E3 泛素连接酶及其在肿瘤发生中的作用。
Front Biosci (Landmark Ed). 2012 Jun 1;17(6):2197-212. doi: 10.2741/4045.
6
CUL4B ubiquitin ligase in mouse development: a model for human X-linked mental retardation syndrome?CUL4B 泛素连接酶在小鼠发育中的作用:人类 X 连锁智力迟钝综合征的模型?
Cell Res. 2012 Aug;22(8):1224-6. doi: 10.1038/cr.2012.79. Epub 2012 May 15.
7
A phase I/II trial of intensity modulated radiation (IMRT) dose escalation with concurrent fixed-dose rate gemcitabine (FDR-G) in patients with unresectable pancreatic cancer.一项强度调制放射治疗(IMRT)剂量递增联合不可切除胰腺癌患者固定剂量率吉西他滨(FDR-G)同步治疗的 I/II 期临床试验。
Int J Radiat Oncol Biol Phys. 2012 Dec 1;84(5):1166-71. doi: 10.1016/j.ijrobp.2012.02.051. Epub 2012 Apr 27.
8
Ras stabilization through aberrant activation of Wnt/β-catenin signaling promotes intestinal tumorigenesis.Ras 通过异常激活 Wnt/β-catenin 信号促进肠道肿瘤发生。
Sci Signal. 2012 Apr 10;5(219):ra30. doi: 10.1126/scisignal.2002242.
9
Inhibition of glycogen synthase kinase-3 activity triggers an apoptotic response in pancreatic cancer cells through JNK-dependent mechanisms.抑制糖原合酶激酶-3 的活性通过 JNK 依赖性机制触发胰腺癌细胞的凋亡反应。
Carcinogenesis. 2012 Mar;33(3):529-37. doi: 10.1093/carcin/bgr309. Epub 2011 Dec 26.
10
Glycogen synthase kinase 3β inhibition sensitizes pancreatic cancer cells to gemcitabine.糖原合酶激酶 3β 抑制使胰腺癌细胞对吉西他滨敏感。
J Gastroenterol. 2012 Mar;47(3):321-33. doi: 10.1007/s00535-011-0484-9. Epub 2011 Nov 1.

胰腺癌中的糖原合酶激酶3β及其在化疗和放疗中的意义。

Glycogen Synthase Kinase 3β in Pancreatic Cancer and its Implications in Chemotherapy and Radiation Therapy.

作者信息

Zhang Qiang, Bhojani Mahaveer S, Ben-Josef Edgar, Spalding Aaron C, Kuick Rork, Sun Yi, Morgan Meredith A

机构信息

Department of Radiation Oncology, University of Michigan Medical School, USA.

Department of Radiation Oncology, University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

J Carcinog Mutagen. 2013 Aug 16;4(3):147. doi: 10.4172/2157-2518.1000147.

DOI:10.4172/2157-2518.1000147
PMID:24944842
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4059685/
Abstract

Pancreatic cancer is a highly lethal disease with a poor prognosis characterized by local and systemic disease progression. Both radiation and chemotherapy play important roles in the management of this disease. However, in order to improve standard therapy many molecularly targeted agents are being developed. Glycogen synthase kinase 3β (GSK3β) participates in a multitude of cellular processes and is a newly proposed therapeutic target in pancreatic cancer. This review will discuss both the oncogenic and tumor suppressor functions of GSK3β in pancreatic cancer with an emphasis on the roles of GSK3β in tumor cell survival and sensitivity to radiation and chemotherapy.

摘要

胰腺癌是一种高度致命的疾病,预后较差,其特征是局部和全身疾病进展。放疗和化疗在这种疾病的治疗中都起着重要作用。然而,为了改进标准疗法,许多分子靶向药物正在研发中。糖原合酶激酶3β(GSK3β)参与多种细胞过程,是胰腺癌中一个新提出的治疗靶点。本综述将讨论GSK3β在胰腺癌中的致癌和抑癌功能,重点是GSK3β在肿瘤细胞存活以及对放疗和化疗敏感性方面的作用。