Radiation-Induced Fibrotic Tumor Microenvironment Regulates Anti-Tumor Immune Response
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Nam, Jae-Kyung | - |
dc.contributor.author | Kim, Ji-Hee | - |
dc.contributor.author | Park, Min-Sik | - |
dc.contributor.author | Kim, Eun Ho | - |
dc.contributor.author | Kim, Joon | - |
dc.contributor.author | Lee, Yoon-Jin | - |
dc.date.accessioned | 2022-02-18T09:40:21Z | - |
dc.date.available | 2022-02-18T09:40:21Z | - |
dc.date.created | 2022-02-08 | - |
dc.date.issued | 2021-10 | - |
dc.identifier.issn | 2072-6694 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/136205 | - |
dc.description.abstract | Simple Summary:& nbsp;Radiation therapy can modulate anti-tumor immune responses. In this study, we investigated the relationship between the anti-tumor immune response and tumor fibrosis after X-ray or neutron radiation therapy. Neutron radiation therapy resulted in lesser fibrosis and greater anti-tumor immunity compared to X-ray irradiation. Radiation therapy-induced fibrotic changes within the tumor environment and tumor regrowth were suppressed by specifically deleting Trp53 in endothelial cells. In particular, the upregulation of PD-L1 expression after X-ray radiation therapy was significantly suppressed via EC-Trp53 deletion. Understanding the effects of different radiation therapy types on the tumor microenvironment provides strategies for enhancing the efficacy of combined radio- and immunotherapy.</p> & nbsp;</p> High linear energy transfer (LET) radiation, such as neutron radiation, is considered more effective for the treatment of cancer than low LET radiation, such as X-rays. We previously reported that X-ray irradiation induced endothelial-to-mesenchymal transition (EndMT) and profibrotic changes, which contributed to the radioresistance of tumors. However, this effect was attenuated in tumors of endothelial-specific Trp53-knockout mice. Herein, we report that compared to X-ray irradiation, neutron radiation therapy reduced collagen deposition and suppressed EndMT in tumors. In addition to the fewer fibrotic changes, more cluster of differentiation (CD8)-positive cytotoxic T cells were observed in neutron-irradiated regrowing tumors than in X-ray-irradiated tumors. Furthermore, lower programmed death-ligand 1 (PD-L1) expression was noted in the former. Endothelial-specific Trp53 deletion suppressed fibrotic changes within the tumor environment following both X-ray and neutron radiation therapy. In particular, the upregulation in PD-L1 expression after X-ray radiation therapy was significantly dampened. Our findings suggest that compared to low LET radiation therapy, high LET radiation therapy can efficiently suppress profibrotic changes and enhance the anti-tumor immune response, resulting in delayed tumor regrowth.</p> | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.subject | ENERGY-TRANSFER RADIATION | - |
dc.subject | TGF-BETA | - |
dc.subject | MESENCHYMAL TRANSITION | - |
dc.subject | IN-VITRO | - |
dc.subject | CANCER | - |
dc.subject | RADIOTHERAPY | - |
dc.subject | INHIBITION | - |
dc.subject | IMMUNOTHERAPY | - |
dc.subject | RADIOBIOLOGY | - |
dc.subject | ACTIVATION | - |
dc.title | Radiation-Induced Fibrotic Tumor Microenvironment Regulates Anti-Tumor Immune Response | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Joon | - |
dc.identifier.doi | 10.3390/cancers13205232 | - |
dc.identifier.scopusid | 2-s2.0-85117164783 | - |
dc.identifier.wosid | 000716939500001 | - |
dc.identifier.bibliographicCitation | CANCERS, v.13, no.20 | - |
dc.relation.isPartOf | CANCERS | - |
dc.citation.title | CANCERS | - |
dc.citation.volume | 13 | - |
dc.citation.number | 20 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | ENERGY-TRANSFER RADIATION | - |
dc.subject.keywordPlus | IMMUNOTHERAPY | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | MESENCHYMAL TRANSITION | - |
dc.subject.keywordPlus | RADIOBIOLOGY | - |
dc.subject.keywordPlus | RADIOTHERAPY | - |
dc.subject.keywordPlus | TGF-BETA | - |
dc.subject.keywordAuthor | X-ray radiation therapy | - |
dc.subject.keywordAuthor | anti-tumor immune response | - |
dc.subject.keywordAuthor | fibrotic tumor microenvironment | - |
dc.subject.keywordAuthor | high linear energy transfer | - |
dc.subject.keywordAuthor | neutron radiation therapy | - |
dc.subject.keywordAuthor | programmed death-ligand 1 | - |
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