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THE INHIBITION OF N-LINKED GLYCOSYLATION BREAKS THE RESISTANACE OF HUMAN OVARIAN CANCER CELLS TO CISPLATIN AND ETOPOSIDE

机译：N-连接的糖基化的抑制破坏了人卵巢癌细胞对顺铂和依托泊苷的抗性

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Glycosylation is found as the most frequent post-translational modification of proteins, frequently altered in tumour cells [1]. Alterations in cellular glycosylation are among the crucial factors involved in cellular signaling, angiogenesis, development and progression of drug resistance in cancer cells. Changes in the expression or activity of glycosylotransferases and in the conformation of peptide backbones are the most important factors, which lead to an increase in the amount of O-GlcNAcylation of intracellular proteins and branched-N-glycans. Abundance of N-glycans correlates not only with the grade of cancer but also with the sensitivity to anticancer treatment [2].

机译：糖基化被发现是蛋白质的最常见的翻译后修饰，经常在肿瘤细胞中改变[1]。细胞糖基化的改变是癌细胞患者患者患有细胞信号传导，血管生成，发育和耐药性的关键因素的关键因素。糖基转移酶的表达或活性的变化和肽骨架的构象是最重要的因素，导致细胞内蛋白和支链-N-聚乙烯的O-GlcNacylation的量增加。丰度N-聚糖不仅与癌症等级相关，而且与对抗癌治疗的敏感性[2]相关联。

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《International Carbohydrate Symposium》|2018年|832 p.|共1页
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Anna Macieia; Joanna Sarnik; Zbigniew J. Witczak;
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中图分类碳水化合物、糖;
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1. Inhibition of N-linked glycosylation by tunicamycin induces E-cadherin-mediated cell-cell adhesion and inhibits cell proliferation in undifferentiated human colon cancer cells. [J] . de Freitas Junior JC, Silva Bdu R, de Souza WF, Cancer chemotherapy and pharmacology. . 2011,第1期

机译：衣霉素对N-联糖基化的抑制作用诱导E-钙粘着蛋白介导的细胞粘附，并抑制未分化的人结肠癌细胞的细胞增殖。
2. Inhibition of N-linked glycosylation by tunicamycin induces E-cadherin-mediated cell–cell adhesion and inhibits cell proliferation in undifferentiated human colon cancer cells [J] . Julio Cesar Madureira de Freitas Junior, Bárbara Du Rocher D’Aguiar Silva, Waldemir Fernandes de Souza, Cancer Chemotherapy and Pharmacology . 2011,第1期

机译：衣霉素对N-联糖基化的抑制作用诱导E-钙黏着蛋白介导的细胞间粘附，并抑制未分化的人类结肠癌细胞的细胞增殖
3. Nanosecond electric pulses induce DNA breaks in cisplatin-sensitive and -resistant human ovarian cancer cells [J] . LinghuL., TanY., LouY., Biochemical and Biophysical Research Communications . 2013,第2期

机译：纳秒电脉冲在顺铂敏感和耐药的人卵巢癌细胞中诱导DNA断裂
4. THE INHIBITION OF N-LINKED GLYCOSYLATION BREAKS THE RESISTANACE OF HUMAN OVARIAN CANCER CELLS TO CISPLATIN AND ETOPOSIDE [C] . Anna Macieia, Joanna Sarnik, Zbigniew J. Witczak International Carbohydrate Symposium . 2018

机译：N-连接的糖基化的抑制破坏了人卵巢癌细胞对顺铂和依托泊苷的抗性
5. E3 Ligase Identified by Differential Display (EDD) Enhances Cell Survival and Cisplatin Resistance in Epithelial Ovarian Cancer and Oral Squamous Cell Carcinoma. [D] . Bradley, Amber Thompson. 2014

机译：通过差异显示（EDD）鉴定的E3连接酶可增强上皮性卵巢癌和口腔鳞状细胞癌的细胞存活率和顺铂耐药性。
6. Activity- and schedule-dependent interactions of paclitaxel etoposide and hydroperoxy-ifosfamide in cisplatin-sensitive and -refractory human ovarian carcinoma cell lines. [O] . U. Klaassen, A. Harstrick, N. Schleucher, 1996

机译：紫杉醇依托泊苷和氢过氧化物-异环磷酰胺在顺铂敏感和难治性人类卵巢癌细胞系中的活性和时间表依赖性相互作用。
7. Akt promotes cisplatin resistance in human ovarian cancer cells through inhibition of p53 phosphorylation and nuclear function [O] . Michael Fraser, Tao Bai, Benjamin K. Tsang 2007

机译：通过抑制P53磷酸化和核功能，促进人卵巢癌细胞中的顺铂抗性

THE INHIBITION OF N-LINKED GLYCOSYLATION BREAKS THE RESISTANACE OF HUMAN OVARIAN CANCER CELLS TO CISPLATIN AND ETOPOSIDE

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