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AKT/GSK3β Signaling in Glioblastoma.胶质母细胞瘤中的AKT/GSK3β信号传导
Neurochem Res. 2017 Mar;42(3):918-924. doi: 10.1007/s11064-016-2044-4. Epub 2016 Aug 27.
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PI3K-mTOR Pathway Inhibition Exhibits Efficacy Against High-grade Glioma in Clinically Relevant Mouse Models.PI3K-mTOR 通路抑制在临床相关的小鼠模型中对高级别脑胶质瘤表现出疗效。
Clin Cancer Res. 2017 Mar 1;23(5):1286-1298. doi: 10.1158/1078-0432.CCR-16-1276. Epub 2016 Aug 23.
3
Clinical utility and treatment outcome of comprehensive genomic profiling in high grade glioma patients.高级别胶质瘤患者综合基因组分析的临床效用和治疗结果
J Neurooncol. 2016 Oct;130(1):211-219. doi: 10.1007/s11060-016-2237-3. Epub 2016 Aug 16.
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Association of MSH6 mutation with glioma susceptibility, drug resistance and progression.MSH6突变与胶质瘤易感性、耐药性及进展的关联
Mol Clin Oncol. 2016 Aug;5(2):236-240. doi: 10.3892/mco.2016.907. Epub 2016 May 20.
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Bioinformatic analyses reveal a distinct Notch activation induced by STAT3 phosphorylation in the mesenchymal subtype of glioblastoma.生物信息学分析揭示了胶质母细胞瘤间质亚型中由 STAT3 磷酸化诱导的 Notch 激活。
J Neurosurg. 2017 Jan;126(1):249-259. doi: 10.3171/2015.11.JNS15432. Epub 2016 Mar 11.
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The Enigma of Rapamycin Dosage.雷帕霉素剂量之谜。
Mol Cancer Ther. 2016 Mar;15(3):347-53. doi: 10.1158/1535-7163.MCT-15-0720. Epub 2016 Feb 25.
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Next generation sequencing approach for detecting 491 fusion genes from human cancer.用于检测人类癌症中491种融合基因的下一代测序方法。
Biomed Res. 2016;37(1):51-62. doi: 10.2220/biomedres.37.51.
8
Aptamer targeting EGFRvIII mutant hampers its constitutive autophosphorylation and affects migration, invasion and proliferation of glioblastoma cells.靶向表皮生长因子受体变体Ⅲ（EGFRvIII）突变体的适体可抑制其组成型自磷酸化，并影响胶质母细胞瘤细胞的迁移、侵袭和增殖。
Oncotarget. 2015 Nov 10;6(35):37570-87. doi: 10.18632/oncotarget.6066.
9
Brain-expressed X-linked 2 Is Pivotal for Hyperactive Mechanistic Target of Rapamycin (mTOR)-mediated Tumorigenesis.脑表达X连锁蛋白2对雷帕霉素机制性靶标（mTOR）介导的肿瘤发生亢进至关重要。
J Biol Chem. 2015 Oct 16;290(42):25756-65. doi: 10.1074/jbc.M115.665208. Epub 2015 Aug 20.
10
NVP-BEZ235, a novel dual PI3K-mTOR inhibitor displays anti-glioma activity and reduces chemoresistance to temozolomide in human glioma cells.NVP-BEZ235，一种新型的双重 PI3K-mTOR 抑制剂，在人神经胶质瘤细胞中显示出抗神经胶质瘤活性，并降低替莫唑胺的化疗耐药性。
Cancer Lett. 2015 Oct 10;367(1):58-68. doi: 10.1016/j.canlet.2015.07.007. Epub 2015 Jul 15.

一种STAT3抑制剂与一种mTOR抑制剂联合对抗替莫唑胺耐药的胶质母细胞瘤细胞系

Combination of a STAT3 Inhibitor and an mTOR Inhibitor Against a Temozolomide-resistant Glioblastoma Cell Line.

作者信息

Miyata Haruo, Ashizawa Tadashi, Iizuka Akira, Kondou Ryota, Nonomura Chizu, Sugino Takashi, Urakami Kenichi, Asai Akira, Hayashi Nakamasa, Mitsuya Koichi, Nakasu Yoko, Yamaguchi Ken, Akiyama Yasuto

机构信息

Immunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka Cancer Center Hospital, Shizuoka, Japan.

Division of Pathology, Shizuoka Cancer Center Hospital, Shizuoka, Japan.

出版信息

Cancer Genomics Proteomics. 2017 Jan 2;14(1):83-91. doi: 10.21873/cgp.20021.

DOI:10.21873/cgp.20021
PMID:28031240
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5267503/
Abstract

BACKGROUND

Temozolomide-resistant (TMZ-R) glioblastoma is very difficult to treat, and a novel approach to overcome resistance is needed.

MATERIALS AND METHODS

The efficacy of a combination treatment of STAT3 inhibitor, STX-0119, with rapamycin was investigated against our established TMZ-resistant U87 cell line.

RESULTS

The growth-inhibitory effect of the combination treatment was significant against the TMZ-R U87 cell line (IC: 78 μM for STX-0119, 30.5 μM for rapamycin and 11.3 μM for combination of the two). Western blotting analysis demonstrated that the inhibitory effect of STX-0119 on S6 and 4E-BP1 activation through regulation of YKL-40 expression occurred in addition to the inhibitory effect of rapamycin against the mTOR pathway.

CONCLUSION

These results suggest that the STAT3 pathway is associated with the mTOR downstream pathway mediated by YKL-40 protein, and the combination therapy of the STAT3 inhibitor and rapamycin could be worth developing as a novel therapeutic approach against TMZ-resistant relapsed gliomas.

摘要

背景

耐替莫唑胺（TMZ-R）的胶质母细胞瘤极难治疗，因此需要一种新的方法来克服耐药性。

材料与方法

研究了STAT3抑制剂STX-0119与雷帕霉素联合治疗对我们建立的耐TMZ的U87细胞系的疗效。

结果

联合治疗对TMZ-R U87细胞系具有显著的生长抑制作用（IC：STX-0119为78μM，雷帕霉素为30.5μM，两者联合为11.3μM）。蛋白质印迹分析表明，除了雷帕霉素对mTOR途径的抑制作用外，STX-0119通过调节YKL-40表达对S6和4E-BP1激活也有抑制作用。

结论

这些结果表明，STAT3途径与由YKL-40蛋白介导的mTOR下游途径相关，STAT3抑制剂与雷帕霉素的联合治疗作为一种针对耐TMZ复发胶质瘤的新治疗方法可能值得开发。