• 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

人结肠癌细胞与单核细胞相互作用后血管生成、转移和信号通路相关因子的动态变化。

Angiogenesis-, metastasis- and signaling pathway-related factor dynamics in human colon cancer cells following interaction with monocytes.

机构信息

Department of Medical Technology, School of Life and Environmental Science, Azabu University, 1-17-71 Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan.

出版信息

Anticancer Res. 2013 Jul;33(7):2895-900.

PMID:23780976
Abstract

BACKGROUND

In tumors, monocytes differentiate into tumor-associated macrophages following interaction with cancer cells. We have previously reported that angiogenesis- and chemotaxis-related factors are associated with human monocyte differentiation following interaction with colon cancer cells. However, the exact nature of factors remains unknown. We investigated factors associated with differentiation of human colon cancer cells following interaction with monocytes.

MATERIALS AND METHODS

The human colon cancer cell line DLD-1 was co-cultured with the human monocyte cell line THP-1. mRNA expression was analyzed by quantitative real-time PCR.

RESULTS

Expression of interleukin-1β, matrix metalloproteinase (MMP)-1, MMP-2, and MMP-3 increased in human colon cancer cells after co-culture with monocytes. Conversely, the expression of monocyte chemotactic protein-1, tumor necrosis factor-α, and signal transducer and activator of transcription-3 did not increase.

CONCLUSION

Differentiation of human colon cancer cells following interaction with monocytes may be associated with angiogenesis and metastasis but not chemotaxis and signaling pathways. Thus, angiogenesis- and metastasis-related factors associated with differentiation of human colon cancer cells may constitute important targets for colon cancer therapy.

摘要

背景

在肿瘤中,单核细胞与癌细胞相互作用后分化为肿瘤相关巨噬细胞。我们之前报道过,与结肠癌细胞相互作用后,与血管生成和趋化相关的因子与人类单核细胞分化有关。然而,确切的因子性质仍不清楚。我们研究了与人类结肠癌细胞在与单核细胞相互作用后分化相关的因子。

材料与方法

将人结肠癌细胞系 DLD-1 与人类单核细胞系 THP-1 共培养。通过实时定量 PCR 分析 mRNA 表达。

结果

与单核细胞共培养后,人结肠癌细胞中白细胞介素 1β、基质金属蛋白酶(MMP)-1、MMP-2 和 MMP-3 的表达增加。相反,单核细胞趋化蛋白 1、肿瘤坏死因子-α 和信号转导和转录激活因子 3 的表达没有增加。

结论

与单核细胞相互作用后人类结肠癌细胞的分化可能与血管生成和转移有关,但与趋化作用和信号通路无关。因此,与人类结肠癌细胞分化相关的血管生成和转移相关因子可能成为结肠癌治疗的重要靶点。

相似文献

1
Angiogenesis-, metastasis- and signaling pathway-related factor dynamics in human colon cancer cells following interaction with monocytes.人结肠癌细胞与单核细胞相互作用后血管生成、转移和信号通路相关因子的动态变化。
Anticancer Res. 2013 Jul;33(7):2895-900.
2
Differential expression of mRNA in human monocytes following interaction with human colon cancer cells.人单核细胞与人结肠癌细胞相互作用后 mRNA 的差异表达。
Anticancer Res. 2011 Jul;31(7):2493-7.
3
Expression of chemotaxis- and angiogenesis-related factors in human monocytes following interaction with colon cancer cells is suppressed by low-dose lipopolysaccharide.低剂量脂多糖抑制人单核细胞与结肠癌细胞相互作用后趋化因子和血管生成相关因子的表达。
Anticancer Res. 2014 Aug;34(8):4609-13.
4
Molecular Response of Human Monocytes Following Interaction with Colon Cancer Cells by Pre-treatment with Low-dose Lipopolysaccharide.低剂量脂多糖预处理后人单核细胞与结肠癌细胞相互作用后的分子反应
Anticancer Res. 2015 Aug;35(8):4473-7.
5
Cross talk between smooth muscle cells and monocytes/activated monocytes via CX3CL1/CX3CR1 axis augments expression of pro-atherogenic molecules.平滑肌细胞与单核细胞/活化单核细胞之间通过CX3CL1/CX3CR1轴的相互作用增强促动脉粥样硬化分子的表达。
Biochim Biophys Acta. 2011 Dec;1813(12):2026-35. doi: 10.1016/j.bbamcr.2011.08.009. Epub 2011 Aug 22.
6
Aloe emodin inhibits colon cancer cell migration/angiogenesis by downregulating MMP-2/9, RhoB and VEGF via reduced DNA binding activity of NF-κB.大黄素通过降低 NF-κB 的 DNA 结合活性来下调 MMP-2/9、RhoB 和 VEGF,从而抑制结肠癌细胞迁移/血管生成。
Eur J Pharm Sci. 2012 Apr 11;45(5):581-91. doi: 10.1016/j.ejps.2011.12.012. Epub 2011 Dec 30.
7
Colon cancer cell-derived tumor necrosis factor-alpha mediates the tumor growth-promoting response in macrophages by up-regulating the colony-stimulating factor-1 pathway.结肠癌细胞衍生的肿瘤坏死因子-α通过上调集落刺激因子-1途径介导巨噬细胞中的肿瘤生长促进反应。
Cancer Res. 2007 Feb 1;67(3):1038-45. doi: 10.1158/0008-5472.CAN-06-2295.
8
Changes in CO2 concentration increase the invasive ability of colon cancer cells.CO2 浓度的变化会增强结肠癌细胞的侵袭能力。
Anticancer Res. 2013 May;33(5):1881-5.
9
Monocyte/macrophage recruitment, activation and differentiation modulate interleukin-8 production: a paracrine role of tumor-associated macrophages in tumor angiogenesis.单核细胞/巨噬细胞的募集、激活和分化调节白细胞介素-8的产生:肿瘤相关巨噬细胞在肿瘤血管生成中的旁分泌作用。
In Vivo. 2002 Nov-Dec;16(6):471-7.
10
Interleukin-1beta and tumor necrosis factor-alpha induce chemokine and matrix metalloproteinase gene expression in human colonic subepithelial myofibroblasts.白细胞介素-1β和肿瘤坏死因子-α诱导人结肠上皮下肌成纤维细胞中趋化因子和基质金属蛋白酶基因表达。
Scand J Gastroenterol. 2002 Mar;37(3):317-24. doi: 10.1080/003655202317284228.

引用本文的文献

1
Oral and transdermal administration of lipopolysaccharide safely enhances self-healing ability through the macrophage network.口服和经皮给予脂多糖可通过巨噬细胞网络安全地增强自我修复能力。
Front Immunol. 2025 Mar 31;16:1563484. doi: 10.3389/fimmu.2025.1563484. eCollection 2025.
2
Expression of pro-angiogenic factors as potential biomarkers in experimental models of colon cancer.促血管生成因子在结肠癌实验模型中的表达作为潜在的生物标志物。
J Cancer Res Clin Oncol. 2020 Jun;146(6):1427-1440. doi: 10.1007/s00432-020-03186-x. Epub 2020 Apr 6.
3
Modulators affecting the immune dialogue between human immune and colon cancer cells.
影响人类免疫细胞与结肠癌细胞之间免疫对话的调节剂。
World J Gastrointest Oncol. 2014 May 15;6(5):129-38. doi: 10.4251/wjgo.v6.i5.129.
4
Over-expression of ARHI decreases tumor growth, migration, and invasion in human glioma.ARHI 的过表达可降低人神经胶质瘤中的肿瘤生长、迁移和侵袭。
Med Oncol. 2014 Mar;31(3):846. doi: 10.1007/s12032-014-0846-2. Epub 2014 Jan 24.
5
Role of matrix metalloproteinases in non-healing venous ulcers.基质金属蛋白酶在难愈性静脉溃疡中的作用
Int Wound J. 2015 Dec;12(6):641-5. doi: 10.1111/iwj.12181. Epub 2013 Oct 24.