• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

更正：巨噬细胞衍生的CCL5通过p65/STAT3-CSN5-PD-L1途径促进结肠癌细胞的免疫逃逸。

Correction: Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway.

作者信息

Liu Chao, Yao Zhaoying, Wang Jianing, Zhang Wen, Yang Yan, Zhang Yan, Qu Xinliang, Zhu Yubing, Zou Jianjun, Peng Sishi, Zhao Yan, Zhao Shuli, He Bangshun, Mi Qiongyu, Liu Xiuting, Zhang Xu, Du Qianming

机构信息

Department of Pharmacy, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, PR China.

Department of Clinical Pharmacy, School of Basic Medicine & Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, PR China.

出版信息

Cell Death Differ. 2020 Jul;27(7):2293. doi: 10.1038/s41418-020-0506-3.

DOI:10.1038/s41418-020-0506-3
PMID:32024980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7413370/
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

摘要

本文的一个修订版本已发表，可通过本文顶部的链接获取。

相似文献

1
Correction: Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway.更正：巨噬细胞衍生的CCL5通过p65/STAT3-CSN5-PD-L1途径促进结肠癌细胞的免疫逃逸。
Cell Death Differ. 2020 Jul;27(7):2293. doi: 10.1038/s41418-020-0506-3.
2
Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway.巨噬细胞衍生的 CCL5 通过 p65/STAT3-CSN5-PD-L1 通路促进结直肠癌细胞的免疫逃逸。
Cell Death Differ. 2020 Jun;27(6):1765-1781. doi: 10.1038/s41418-019-0460-0. Epub 2019 Dec 4.
3
Author Correction: PD-L1-mediated gasdermin C expression switches apoptosis to pyroptosis in cancer cells and facilitates tumour necrosis.作者更正：PD-L1介导的gasdermin C表达使癌细胞中的凋亡转变为焦亡，并促进肿瘤坏死。
Nat Cell Biol. 2020 Nov;22(11):1396. doi: 10.1038/s41556-020-00599-1.
4
Correction to: Long non-coding RNA HOTTIP enhances IL-6 expression to potentiate immune escape of ovarian cancer cells by upregulating the expression of PD-L1 in neutrophils.对《长链非编码RNA HOTTIP通过上调中性粒细胞中PD-L1的表达增强IL-6表达以促进卵巢癌细胞免疫逃逸》一文的更正
J Exp Clin Cancer Res. 2020 Dec 4;39(1):272. doi: 10.1186/s13046-020-01755-z.
5
Author Correction: Cyclin D-CDK4 kinase destabilizes PD-L1 via cullin 3-SPOP to control cancer immune surveillance.作者更正：细胞周期蛋白D - 细胞周期蛋白依赖性激酶4通过cullin 3 - SPOP使程序性死亡蛋白1配体（PD - L1）不稳定以控制癌症免疫监视。
Nature. 2019 Jul;571(7766):E10. doi: 10.1038/s41586-019-1351-8.
6
Author Correction: Real-world evidence and clinical observations of the treatment of advanced non-small cell lung cancer with PD-1/PD-L1 inhibitors.作者更正：PD-1/PD-L1抑制剂治疗晚期非小细胞肺癌的真实世界证据及临床观察
Sci Rep. 2020 Jan 27;10(1):1525. doi: 10.1038/s41598-020-58487-5.
7
FGFR2 Promotes Expression of PD-L1 in Colorectal Cancer via the JAK/STAT3 Signaling Pathway.成纤维细胞生长因子受体 2 通过 JAK/STAT3 信号通路促进结直肠癌中 PD-L1 的表达。
J Immunol. 2019 May 15;202(10):3065-3075. doi: 10.4049/jimmunol.1801199. Epub 2019 Apr 12.
8
Author Correction: Drug-induced PD-L1 expression and cell stress response in breast cancer cells can be balanced by drug combination.作者更正：乳腺癌细胞中药物诱导的PD-L1表达和细胞应激反应可通过联合用药实现平衡。
Sci Rep. 2020 Mar 5;10(1):4463. doi: 10.1038/s41598-020-60964-w.
9
Author Correction: Meteorin-like facilitates skeletal muscle repair through a Stat3/IGF-1 mechanism.作者更正：类 Meteorin 通过 Stat3/IGF-1 机制促进骨骼肌修复。
Nat Metab. 2020 Aug;2(8):794. doi: 10.1038/s42255-020-0257-y.
10
Author Correction: High PD-L1 expression is associated with therapeutic response to pembrolizumab in patients with advanced biliary tract cancer.作者更正：高程序性死亡受体配体1（PD-L1）表达与晚期胆管癌患者对帕博利珠单抗的治疗反应相关。
Sci Rep. 2020 Dec 3;10(1):21552. doi: 10.1038/s41598-020-78512-x.

引用本文的文献

1
TRIM26 deficiency potentially suppresses colorectal cancer liver metastasis through NF-κB-mediated M1-like tumor-associated macrophage polarization.TRIM26缺陷可能通过NF-κB介导的M1样肿瘤相关巨噬细胞极化抑制结直肠癌肝转移。
Br J Cancer. 2025 Jun 9. doi: 10.1038/s41416-025-03072-8.
2
GOLM1 dictates acquired Lenvatinib resistance by a GOLM1-CSN5 positive feedback loop upon EGFR signaling activation in hepatocellular carcinoma.GOLM1 通过 EGFR 信号激活在肝细胞癌中形成 GOLM1-CSN5 正反馈环来决定获得性仑伐替尼耐药性。
Oncogene. 2024 Oct;43(42):3108-3120. doi: 10.1038/s41388-024-03153-7. Epub 2024 Sep 9.
3
Crosstalk between gut microbiota and metastasis in colorectal cancer: implication of neutrophil extracellular traps.结直肠癌中肠道微生物群与转移的串扰：中性粒细胞胞外陷阱的作用。
Front Immunol. 2023 Oct 23;14:1296783. doi: 10.3389/fimmu.2023.1296783. eCollection 2023.
4
The regulatory network of the chemokine CCL5 in colorectal cancer.结直肠癌中趋化因子 CCL5 的调控网络。
Ann Med. 2023 Dec;55(1):2205168. doi: 10.1080/07853890.2023.2205168.
5
Current insight into the regulation of PD-L1 in cancer.当前对癌症中程序性死亡受体配体1（PD-L1）调控的见解。
Exp Hematol Oncol. 2022 Jul 30;11(1):44. doi: 10.1186/s40164-022-00297-8.
6
Immunotherapy as a Therapeutic Strategy for Gastrointestinal Cancer-Current Treatment Options and Future Perspectives.免疫疗法作为胃肠道癌症的治疗策略——当前的治疗选择和未来的展望。
Int J Mol Sci. 2022 Jun 15;23(12):6664. doi: 10.3390/ijms23126664.