{"title":"RNF200通过调节肺癌肿瘤相关巨噬细胞中PD-L1的稳定性来增强放疗敏感性。","authors":"Hongbo Xu, Feng Cai, Lu Xu, Dengsheng Jiang, Gengming Wang, Xianwen Zhang, Yajun Zhang","doi":"10.62347/BIQP4822","DOIUrl":null,"url":null,"abstract":"<p><p>Radiotherapy is a cornerstone treatment for lung cancer; however, enhancing its efficacy and overcoming immune escape mechanisms - particularly those mediated by tumor-associated macrophages (TAMs) expressing programmed death-ligand 1 (PD-L1) - remain significant challenges. The E3 ubiquitin ligase RNF200 has been implicated in the regulation of PD-L1 expression, yet its role in the context of radiotherapy is not well understood. To address this, non-small cell lung cancer (NSCLC) tissue samples from patients with and without prior radiotherapy were analyzed for RNF200 and PD-L1 expression using quantitative RT-PCR and Western blotting. Additionally, RAW264.7 macrophages were subjected to ionizing radiation and genetically manipulated to assess the impact of RNF200 on PD-L1 expression and stability through co-immunoprecipitation and ubiquitination assays. Co-culture experiments with macrophages and lung cancer cells were performed to evaluate the influence of RNF200 on radiotherapy sensitivity. In NSCLC tissues and macrophages, radiotherapy was found to downregulate RNF200 expression while upregulating PD-L1 expression. Overexpression of RNF200 led to marked suppression of PD-L1 expression, whereas RNF200 knockdown produced the opposite effect. Co-immunoprecipitation and ubiquitination assays revealed that RNF200 physically interacted with PD-L1 and promoted its polyubiquitination and proteasomal degradation. Furthermore, co-culture studies demonstrated that macrophages overexpressing RNF200 enhanced the sensitivity of lung cancer cells to radiotherapy, as evidenced by reduced proliferation, increased necrosis, and decreased secretion of transforming growth factor beta TGF-β. Collectively, these findings indicate that RNF200 enhances radiotherapy sensitivity in lung cancer by regulating PD-L1 expression through ubiquitination. Targeting RNF200 may represent a promising strategy to improve the efficacy of radiotherapy in lung cancer treatment.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 8","pages":"3449-3459"},"PeriodicalIF":2.9000,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432579/pdf/","citationCount":"0","resultStr":"{\"title\":\"RNF200 enhances radiotherapy sensitivity by modulating PD-L1 stability in tumor-associated macrophages of lung cancer.\",\"authors\":\"Hongbo Xu, Feng Cai, Lu Xu, Dengsheng Jiang, Gengming Wang, Xianwen Zhang, Yajun Zhang\",\"doi\":\"10.62347/BIQP4822\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Radiotherapy is a cornerstone treatment for lung cancer; however, enhancing its efficacy and overcoming immune escape mechanisms - particularly those mediated by tumor-associated macrophages (TAMs) expressing programmed death-ligand 1 (PD-L1) - remain significant challenges. The E3 ubiquitin ligase RNF200 has been implicated in the regulation of PD-L1 expression, yet its role in the context of radiotherapy is not well understood. To address this, non-small cell lung cancer (NSCLC) tissue samples from patients with and without prior radiotherapy were analyzed for RNF200 and PD-L1 expression using quantitative RT-PCR and Western blotting. Additionally, RAW264.7 macrophages were subjected to ionizing radiation and genetically manipulated to assess the impact of RNF200 on PD-L1 expression and stability through co-immunoprecipitation and ubiquitination assays. Co-culture experiments with macrophages and lung cancer cells were performed to evaluate the influence of RNF200 on radiotherapy sensitivity. In NSCLC tissues and macrophages, radiotherapy was found to downregulate RNF200 expression while upregulating PD-L1 expression. Overexpression of RNF200 led to marked suppression of PD-L1 expression, whereas RNF200 knockdown produced the opposite effect. Co-immunoprecipitation and ubiquitination assays revealed that RNF200 physically interacted with PD-L1 and promoted its polyubiquitination and proteasomal degradation. Furthermore, co-culture studies demonstrated that macrophages overexpressing RNF200 enhanced the sensitivity of lung cancer cells to radiotherapy, as evidenced by reduced proliferation, increased necrosis, and decreased secretion of transforming growth factor beta TGF-β. Collectively, these findings indicate that RNF200 enhances radiotherapy sensitivity in lung cancer by regulating PD-L1 expression through ubiquitination. Targeting RNF200 may represent a promising strategy to improve the efficacy of radiotherapy in lung cancer treatment.</p>\",\"PeriodicalId\":7437,\"journal\":{\"name\":\"American journal of cancer research\",\"volume\":\"15 8\",\"pages\":\"3449-3459\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-08-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432579/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of cancer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/BIQP4822\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/BIQP4822","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
RNF200 enhances radiotherapy sensitivity by modulating PD-L1 stability in tumor-associated macrophages of lung cancer.
Radiotherapy is a cornerstone treatment for lung cancer; however, enhancing its efficacy and overcoming immune escape mechanisms - particularly those mediated by tumor-associated macrophages (TAMs) expressing programmed death-ligand 1 (PD-L1) - remain significant challenges. The E3 ubiquitin ligase RNF200 has been implicated in the regulation of PD-L1 expression, yet its role in the context of radiotherapy is not well understood. To address this, non-small cell lung cancer (NSCLC) tissue samples from patients with and without prior radiotherapy were analyzed for RNF200 and PD-L1 expression using quantitative RT-PCR and Western blotting. Additionally, RAW264.7 macrophages were subjected to ionizing radiation and genetically manipulated to assess the impact of RNF200 on PD-L1 expression and stability through co-immunoprecipitation and ubiquitination assays. Co-culture experiments with macrophages and lung cancer cells were performed to evaluate the influence of RNF200 on radiotherapy sensitivity. In NSCLC tissues and macrophages, radiotherapy was found to downregulate RNF200 expression while upregulating PD-L1 expression. Overexpression of RNF200 led to marked suppression of PD-L1 expression, whereas RNF200 knockdown produced the opposite effect. Co-immunoprecipitation and ubiquitination assays revealed that RNF200 physically interacted with PD-L1 and promoted its polyubiquitination and proteasomal degradation. Furthermore, co-culture studies demonstrated that macrophages overexpressing RNF200 enhanced the sensitivity of lung cancer cells to radiotherapy, as evidenced by reduced proliferation, increased necrosis, and decreased secretion of transforming growth factor beta TGF-β. Collectively, these findings indicate that RNF200 enhances radiotherapy sensitivity in lung cancer by regulating PD-L1 expression through ubiquitination. Targeting RNF200 may represent a promising strategy to improve the efficacy of radiotherapy in lung cancer treatment.
期刊介绍:
The American Journal of Cancer Research (AJCR) (ISSN 2156-6976), is an independent open access, online only journal to facilitate rapid dissemination of novel discoveries in basic science and treatment of cancer. It was founded by a group of scientists for cancer research and clinical academic oncologists from around the world, who are devoted to the promotion and advancement of our understanding of the cancer and its treatment. The scope of AJCR is intended to encompass that of multi-disciplinary researchers from any scientific discipline where the primary focus of the research is to increase and integrate knowledge about etiology and molecular mechanisms of carcinogenesis with the ultimate aim of advancing the cure and prevention of this increasingly devastating disease. To achieve these aims AJCR will publish review articles, original articles and new techniques in cancer research and therapy. It will also publish hypothesis, case reports and letter to the editor. Unlike most other open access online journals, AJCR will keep most of the traditional features of paper print that we are all familiar with, such as continuous volume, issue numbers, as well as continuous page numbers to retain our comfortable familiarity towards an academic journal.