دورية أكاديمية

CD133-containing microvesicles promote cancer progression by inducing M2-like tumor-associated macrophage polarization in the tumor microenvironment of colorectal cancer.

التفاصيل البيبلوغرافية
العنوان: CD133-containing microvesicles promote cancer progression by inducing M2-like tumor-associated macrophage polarization in the tumor microenvironment of colorectal cancer.
المؤلفون: Kim SY; Division of Life Sciences, Korea University, Seoul 02841, South Korea., Park S; Division of Life Sciences, Korea University, Seoul 02841, South Korea., Kim S; Division of Life Sciences, Korea University, Seoul 02841, South Korea., Ko J; Division of Life Sciences, Korea University, Seoul 02841, South Korea.
المصدر: Carcinogenesis [Carcinogenesis] 2024 May 19; Vol. 45 (5), pp. 300-310.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Irl Press At Oxford University Press Country of Publication: England NLM ID: 8008055 Publication Model: Print Cited Medium: Internet ISSN: 1460-2180 (Electronic) Linking ISSN: 01433334 NLM ISO Abbreviation: Carcinogenesis Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford : Irl Press At Oxford University Press
Original Publication: [New York, IRL Press]
مواضيع طبية MeSH: Tumor Microenvironment*/immunology , Colorectal Neoplasms*/pathology , Colorectal Neoplasms*/immunology , Colorectal Neoplasms*/metabolism , AC133 Antigen*/metabolism , Tumor-Associated Macrophages*/metabolism , Tumor-Associated Macrophages*/immunology , Disease Progression*, Humans ; Cell-Derived Microparticles/metabolism ; Epithelial-Mesenchymal Transition ; Cell Proliferation ; STAT3 Transcription Factor/metabolism ; Cell Movement ; Animals ; Mice ; Cell Line, Tumor ; Interleukin-6/metabolism
مستخلص: Tumor-associated macrophages (TAMs) are among the most abundant cell types in the tumor microenvironment (TME). The immunosuppressive TME formed by TAMs is an essential prerequisite for cancer progression. Tumor-derived microvesicles (MVs), a subtype of extracellular vesicle shed directly from the plasma membrane, are important regulators of intercellular communication and TME modulation during tumorigenesis. However, the exact mechanism by which tumor-derived MVs induce the generation of the immunosuppressive TME and polarization of TAMs remains unclear. Here, we investigated the role of CD133-containing MVs derived from colorectal cancer (CRC) cells in macrophage polarization and cancer progression. CD133-containing MVs from CRC cells were incorporated into macrophages, and M0 macrophages were morphologically transformed into M2-like TAMs. CD133-containing MVs were found to increase the mRNA expression of M2 macrophage markers. Additionally, cytokine array analysis revealed that M2-like TAMs induced by CD133-containing MVs increased the secretion of interleukin 6, which activated the STAT3 pathway in CRC cells. Furthermore, the conditioned medium of M2-like TAMs promoted cell motility, epithelial-mesenchymal transition, and cell proliferation. However, MVs from CD133-knockdown cells had little effect on TAM polarization and CRC progression. These results demonstrate that CD133-containing MVs induce M2-like TAM polarization and contribute to cancer progression by mediating crosstalk between tumor cells and TAMs in the TME of CRC.
(© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)
معلومات مُعتمدة: 2015R1A5A1009024 Tunneling Nanotube Research Center; National Research Foundation of Korea; Korea Government; Korea University
المشرفين على المادة: 0 (PROM1 protein, human)
0 (STAT3 protein, human)
تواريخ الأحداث: Date Created: 20231212 Date Completed: 20240519 Latest Revision: 20240528
رمز التحديث: 20240528
DOI: 10.1093/carcin/bgad093
PMID: 38085813
قاعدة البيانات: MEDLINE
الوصف
تدمد:1460-2180
DOI:10.1093/carcin/bgad093