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本文引用的文献

1
Role of Autophagy in Capsaicin-Induced Apoptosis in U251 Glioma Cells.自噬在辣椒素诱导U251胶质瘤细胞凋亡中的作用
Cell Mol Neurobiol. 2016 Jul;36(5):737-43. doi: 10.1007/s10571-015-0254-y. Epub 2015 Sep 9.
2
Autophagy and lysosomal related protein expression patterns in human glioblastoma.人胶质母细胞瘤中自噬及溶酶体相关蛋白表达模式
Cancer Biol Ther. 2014;15(11):1468-78. doi: 10.4161/15384047.2014.955719.
3
Clinical significance of autophagic protein LC3 levels and its correlation with XIAP expression in hepatocellular carcinoma.自噬蛋白LC3水平在肝细胞癌中的临床意义及其与XIAP表达的相关性
Med Oncol. 2014 Aug;31(8):108. doi: 10.1007/s12032-014-0108-3. Epub 2014 Jul 9.
4
Prognostic significance of p62/SQSTM1 subcellular localization and LC3B in oral squamous cell carcinoma.p62/SQSTM1 亚细胞定位和 LC3B 在口腔鳞状细胞癌中的预后意义。
Br J Cancer. 2014 Aug 26;111(5):944-54. doi: 10.1038/bjc.2014.355. Epub 2014 Jul 1.
5
Correlation of altered expression of the autophagy marker LC3B with poor prognosis in astrocytoma.自噬标记物 LC3B 表达改变与星形细胞瘤不良预后的相关性。
Biomed Res Int. 2014;2014:723176. doi: 10.1155/2014/723176. Epub 2014 May 12.
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The residual tumor autophagy marker LC3B serves as a prognostic marker in local advanced breast cancer after neoadjuvant chemotherapy.残余肿瘤自噬标志物 LC3B 可作为新辅助化疗后局部晚期乳腺癌的预后标志物。
Clin Cancer Res. 2013 Dec 15;19(24):6853-62. doi: 10.1158/1078-0432.CCR-13-1617. Epub 2013 Oct 18.
7
Association of p62/SQSTM1 excess and oral carcinogenesis.p62/SQSTM1 过剩与口腔癌发生的关联。
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8
Knockdown of p62/sequestosome 1 attenuates autophagy and inhibits colorectal cancer cell growth.敲低 p62/自噬体 1 可抑制自噬并抑制结直肠癌细胞生长。
Mol Cell Biochem. 2014 Jan;385(1-2):95-102. doi: 10.1007/s11010-013-1818-0. Epub 2013 Sep 25.
9
The autophagy protein LC3A correlates with hypoxia and is a prognostic marker of patient survival in clear cell ovarian cancer.自噬蛋白LC3A与缺氧相关,是透明细胞卵巢癌患者生存的预后标志物。
J Pathol. 2012 Dec;228(4):437-47. doi: 10.1002/path.4090.
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Microtubule-associated protein 1 light chain 3 (LC3) interacts with Bnip3 protein to selectively remove endoplasmic reticulum and mitochondria via autophagy.微管相关蛋白 1 轻链 3(LC3)与 Bnip3 蛋白相互作用,通过自噬选择性地去除内质网和线粒体。
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对胶质瘤患者自噬蛋白LC3B和p62水平的免疫组织化学评估。

Immunohistochemical assessment of autophagic protein LC3B and p62 levels in glioma patients.

作者信息

Jiang Tao, Wu Zhengsheng

机构信息

Department of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University Hefei, Anhui, China.

Department of Pathology, Anhui Medical University Hefei, Anhui, China.

出版信息

Int J Clin Exp Pathol. 2018 Feb 1;11(2):862-868. eCollection 2018.

PMID:31938176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6958015/
Abstract

Glioma is a serious malignant central nervous system disease. Autophagy is a basic cellular catabolic mechanism maintaining the cellular homeostasis through degradation of unnecessary molecules and components and reusing them. Autophagy also promotes development, progression and anticancer therapy resistance of many types of human cancers. In this study, we detected the expression of two autophagic protein LC3B and p62 in 81 glioma tissues by immunohistochemistry analysis. LC3B and p62 was highly expressed in high-grade glioma tissues, compared with low-grade glioma tissues. High levels of LC3B and p62 protein were also associated with advanced tumor stages, worse relapse-free survival (RFS) and overall survival (OS) in glioma patients, but not with patients' age, gender or KPS. Additionally, there was a statistically positive correlation between the expression of LC3B and p62 in glioma tissues. Therefore, we determined LC3B and p62 which contributed to autophagy behavior promoted development and poor prognosis of malignant gliomas. Therapeutic methods based on autophagy or targeting LC3B or p62 may be considered as a potential therapeutic strategy to retard progression of malignant gliomas.

摘要

胶质瘤是一种严重的中枢神经系统恶性疾病。自噬是一种基本的细胞分解代谢机制,通过降解不必要的分子和成分并重新利用它们来维持细胞内稳态。自噬还促进多种人类癌症的发生、发展及抗癌治疗耐药性。在本研究中,我们通过免疫组织化学分析检测了81例胶质瘤组织中两种自噬蛋白LC3B和p62的表达。与低级别胶质瘤组织相比,LC3B和p62在高级别胶质瘤组织中高表达。LC3B和p62蛋白的高水平还与胶质瘤患者的肿瘤晚期、无复发生存期(RFS)和总生存期(OS)较差相关,但与患者的年龄、性别或KPS无关。此外,胶质瘤组织中LC3B和p62的表达之间存在统计学上的正相关。因此,我们确定了有助于自噬行为的LC3B和p62促进了恶性胶质瘤的发展和不良预后。基于自噬或靶向LC3B或p62的治疗方法可能被视为延缓恶性胶质瘤进展的潜在治疗策略。