• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文OA文献 >Deciphering the Elevated Lipid via CD36 in Mantle Cell Lymphoma with Bortezomib Resistance Using Synchrotron-Based Fourier Transform Infrared Spectroscopy of Single Cells
【2h】

Deciphering the Elevated Lipid via CD36 in Mantle Cell Lymphoma with Bortezomib Resistance Using Synchrotron-Based Fourier Transform Infrared Spectroscopy of Single Cells

机译：通过使用Synchrotron的傅里叶变换的单细胞的傅里叶傅里叶变换红外光谱分式通过CD36通过CD36通过CD36通过CD36通过CD36来解开升高的脂质

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Despite overall progress in improving cancer treatments, the complete response of mantle cell lymphoma (MCL) is still limited due to the inevitable development of drug resistance. More than half of patients did not attain response to bortezomib (BTZ), the approved treatment for relapsed or refractory MCL. Understanding how MCL cells acquire BTZ resistance at the molecular level may be a key to the long-term management of MCL patients and new therapeutic strategies. We established a series of de novo BTZ-resistant human MCL-derived cells with approximately 15- to 60-fold less sensitivity than those of parental cells. Using gene expression profiling, we discovered that putative cancer-related genes involved in drug resistance and cell survival tested were mostly downregulated, likely due to global DNA hypermethylation. Significant information on dysregulated lipid metabolism was obtained from synchrotron-based Fourier transform infrared (FTIR) spectroscopy of single cells. We demonstrated for the first time an upregulation of CD36 in highly BTZ-resistant cells in accordance with an increase in their lipid accumulation. Ectopic expression of CD36 causes an increase in lipid droplets and renders BTZ resistance to various human MCL cells. By contrast, inhibition of CD36 by neutralizing antibody strongly enhances BTZ sensitivity, particularly in CD36-overexpressing cells and de novo BTZ-resistant cells. Together, our findings highlight the potential application of CD36 inhibition for BTZ sensitization and suggest the use of FTIR spectroscopy as a promising technique in cancer research.
机译：尽管在改善癌症治疗方面进行了总体进展，但由于耐药性不可避免地发展，裂缝细胞淋巴瘤（MCL）的完全反应仍然有限。超过一半的患者没有获得对Bortezomib（BTZ）的反应，对复发或难治性MCL的批准处理。了解MCL细胞如何在分子水平上获得BTZ抗性可能是MCL患者长期管理的关键和新的治疗策略。我们建立了一系列Novo BTZ的人MCL衍生的细胞，其敏感性大约比亲本细胞的敏感性大约15-至60倍。使用基因表达分析，我们发现涉及耐药性和细胞存活的推定癌症相关基因大多下调，可能由于全球DNA高甲基化。从单细胞的同步辐射傅里叶变换红外（FTIR）光谱法获得了关于失调脂质代谢的重要信息。我们首次证明了根据其脂质积累的增加，第一次在高度BTZ抗性细胞中上调CD36。 CD36的异位表达导致脂液滴增加，使BTZ抗BTZ抗性对各种人MCL细胞。相比之下，通过中和抗体的抑制强烈地增强了BTZ敏感性，特别是在CD36过表达细胞和De Novo BTZ细胞中。我们的研究结果共同突出了CD36抑制对BTZ敏化的潜在应用，并表明FTIR光谱用途作为癌症研究中有前途的技术。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号