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Exosome derived from epigallocatechin gallate treated breast cancer cells suppresses tumor growth by inhibiting tumor-associated macrophage infiltration and M2 polarization
DC Field | Value | Language |
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dc.contributor.author | Jang, Ji-Young | - |
dc.contributor.author | Lee, Jong-Kuen | - |
dc.contributor.author | Jeon, Yoon-Kyung | - |
dc.contributor.author | Kim, Chul-Woo | - |
dc.date.accessioned | 2013-10-04T01:27:14Z | - |
dc.date.available | 2013-10-04T01:27:14Z | - |
dc.date.issued | 2013-09-17 | - |
dc.identifier.citation | BMC Cancer Vol.13 No.421 pp. 1-12 | ko_KR |
dc.identifier.issn | 1471-2407 | - |
dc.identifier.uri | https://hdl.handle.net/10371/83513 | - |
dc.identifier.uri | http://www.biomedcentral.com/1471-2407/13/421 | - |
dc.description.abstract | Background : Tumor-associated macrophages (TAM) play an important role in tumor microenvironment. Particularly, M2 macrophages contribute to tumor progression, depending on the expression of NF-κB. Tumor-derived exosomes can modulate tumor microenvironment by transferring miRNAs to immune cells. Epigallocatechin gallate (EGCG) has well known anti-tumor effects; however, no data are available on the influence of EGCG on communication with cancer cells and TAM.
Methods : Murine breast cancer cell lines, 4T1, was used for in vivo and ex vivo studies. Exosome was extracted from EGCG-treated 4T1 cells, and the change of miRNAs was screened using microarray. Tumor cells or TAM isolated from murine tumor graft were incubated with exosomes derived from EGCG-treated and/or miR-16 inhibitor-transfected 4T1 cells. Chemokines for monocytes (CSF-1 and CCL-2), cytokines both with high (IL-6 and TGF-β) and low (TNF-α) expression in M2 macrophages, and molecules in NF-κB pathway (IKKα and Iκ-B) were evaluated by RT-qPCR or western blot. Results : EGCG suppressed tumor growth in murine breast cancer model, which was associated with decreased TAM and M2 macrophage infiltration. Expression of chemokine for monocytes (CSF-1 and CCL-2) were low in tumor cells from EGCG-treated mice, and cytokines of TAM was skewed from M2- into M1-like phenotype by EGCG as evidenced by decreased IL-6 and TGF-β and increased TNF-α. Ex vivo incubation of isolated tumor cells with EGCG inhibited the CSF-1 and CCL-2 expression. Ex vivo incubation of TAM with exosomes from EGCG-treated 4T1 cells led to IKKα suppression and concomitant I-κB accumulation; increase of IL-6 and TGF-β; and, decrease of TNF-α. EGCG up-regulated miR-16 in 4T1 cells and in the exosomes. Treatment of tumor cells or TAM with exosomes derived from EGCG-treated and miR-16-knock-downed 4T1 cells restored the above effects on chemokines, cytokines, and NF-κB pathway elicited by EGCG-treated exosomes. Conclusions : Our data demonstrate that EGCG up-regulates miR-16 in tumor cells, which can be transferred to TAM via exosomes and inhibits TAM infiltration and M2 polarization. We suggest a novel mechanism by which EGCG exerts anti-tumor activity via regulation of TAM in tumor microenvironment. | ko_KR |
dc.description.sponsorship | This work was supported by the Global Core Research Center (GCRC) grant (No. 2012–0001190) from the National Research Foundation (NRF), Ministry of Education, Science and Technology (MEST) (Republic of Korea). | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BioMed Central Ltd. | ko_KR |
dc.subject | EGCG | ko_KR |
dc.subject | Exosomes | ko_KR |
dc.subject | miR-16 | ko_KR |
dc.subject | Tumor microenvironment | ko_KR |
dc.subject | Tumor-associated macrophages (TAM) | ko_KR |
dc.title | Exosome derived from epigallocatechin gallate treated breast cancer cells suppresses tumor growth by inhibiting tumor-associated macrophage infiltration and M2 polarization | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 장지영 | - |
dc.contributor.AlternativeAuthor | 이종근 | - |
dc.contributor.AlternativeAuthor | 전윤경 | - |
dc.contributor.AlternativeAuthor | 김철우 | - |
dc.identifier.doi | 10.1186/1471-2407-13-421 | - |
dc.language.rfc3066 | en | - |
dc.description.version | Peer Reviewed | - |
dc.rights.holder | Ji-Young Jang et al.; licensee BioMed Central Ltd. | - |
dc.date.updated | 2013-10-03T08:53:26Z | - |
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