Cancer Biology & Medicine最新文献

{"title":"Mitochondrial transplantation sensitizes chemotherapy to inhibit tumor development by enhancing anti-tumor immunity.","authors":"Shumeng Lin, Liuliu Yuan, Xiao Chen, Shiyin Chen, Mengling Wei, Bingjie Hao, Tiansheng Zheng, Lihong Fan","doi":"10.20892/j.issn.2095-3941.2024.0596","DOIUrl":"10.20892/j.issn.2095-3941.2024.0596","url":null,"abstract":"<p><strong>Objective: </strong>Lung cancer is the leading cause of cancer-related deaths worldwide. Chemotherapy is associated with side effects, such as damage to myeloid cells and a reduction in the number of immune cells in patients. In addition, tumor cells hijack the mitochondria of immune cells through tunnel nanotubes, thereby weakening immune ability.</p><p><strong>Methods: </strong>In this study the effects of direct mitochondria transplantation on cancer cell proliferation and chemotherapeutic sensitivity were determined, as well as anti-tumor immunity in <i>in vitro</i> and <i>in vivo</i> lung cancer models.</p><p><strong>Results: </strong>A combination of mitochondrial transplantation and cisplatin chemotherapy was shown for the first time to significantly improve immune infiltration of advanced non-small cell lung cancer (NSCLC) and overcome the shortcomings of cisplatin chemotherapy, including damage to myeloid cells and a reduction in the number of immune cells.</p><p><strong>Conclusions: </strong>The findings of the current study provide valuable recommendations for enhancing immune infiltration and augmenting anti-tumor efficacy during chemotherapy in advanced NSCLC. In addition, the findings support \"mitochondrial transfer\" as a novel paradigm in tumor treatment.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mechanisms and clinical significance of CD8⁺ T cell exhaustion in anti-tumor immunity.","authors":"Tao Zhong, Shuo Sun, Mingsheng Zhao, Bin Zhang, Huabao Xiong","doi":"10.20892/j.issn.2095-3941.2024.0628","DOIUrl":"10.20892/j.issn.2095-3941.2024.0628","url":null,"abstract":"<p><p>CD8⁺ T cell exhaustion, a critical challenge in the immune response to cancer, is characterized by a profound decline in the functionality of effector CD8⁺ T cells. This state of exhaustion is accompanied by the upregulation of various inhibitory receptors and significant shifts in both transcriptional and epigenetic profiles, thus ultimately leading to inadequate tumor control. Therapeutic strategies aimed at reversing CD8⁺ T cell exhaustion have the potential to rejuvenate immune responses and enhance treatment efficacy. This review compiles current knowledge regarding the molecular mechanisms underlying CD8⁺ T cell exhaustion, including the roles of immune checkpoint molecules, the tumor microenvironment, metabolic reprogramming, transcription factors, and epigenetic modifications. Emerging therapeutic approaches designed to combat CD8⁺ T cell exhaustion are evaluated, with emphasis on the modulation of immune checkpoints; targeting of metabolic and transcriptional changes; and exploration of other innovative strategies, such as epigenetic editing and engineered CAR-T cells. Importantly, we expand the exhaustion concept to immune cells beyond CD8⁺ T cells, such as CD4⁺ T cells, natural killer cells, and myeloid populations, thereby highlighting the broader implications of systemic immunosuppression in the cancer context. Finally, we propose avenues for future research aimed at further elucidating the factors and molecular mechanisms associated with CD8⁺ T cell exhaustion, thereby underscoring the critical need for strategies aimed at reversing this state to improve outcomes in cancer immunotherapy.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer cell-derived migrasomes harboring ATF6 promote breast cancer brain metastasis <i>via</i> endoplasmic reticulum stress-mediated disruption of the blood-brain barrier.","authors":"Song Wang, Guohao Gu, Xinmiao Xian, Jun Li, Di Zhang, Jianran Guo, Anqi Zhang, Shen Chen, Dong Yan, Bingwu Yang, Meng An, Wei Zhang, Bo Fu","doi":"10.20892/j.issn.2095-3941.2025.0014","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0014","url":null,"abstract":"<p><strong>Objective: </strong>Migrasomes, an emerging class of migration-facilitating membranous extracellular vesicles, remain largely uncharted in the intricate landscape of tumor metastasis. This study aimed to illuminate the roles and mechanisms underlying cancer cell-derived migrasomes in breast cancer brain metastasis (BCBM).</p><p><strong>Methods: </strong>Migrasomes were isolated and purified from BCBM cells (231-BR) and non-specific organotropic parental counterparts (MDA-MB-231), specifically designated as Mig-BCBM and Mig-BC, respectively. The role of Mig-BCBM in BCBM was investigated using an <i>in vitro</i> endothelial cell layer permeability model and a BCBM mouse model. The regulatory mechanism underlying Mig-BCBM was assessed using RT-qPCR, western blotting, immunofluorescence, <i>ex vivo</i> fluorescence imaging, and a series of rescue experiments.</p><p><strong>Results: </strong>Mig-BCBM potently augmented the permeability of vascular endothelial layers, which facilitated the efficient migration of 231-BR cells across endothelial barriers <i>in vitro</i>. The administration of Mig-BCBM significantly disrupted the blood-brain barrier (BBB) and accelerated BCBM progression <i>in vivo</i>, as evidenced in mouse models, compared to the Mig-BC and control groups. Mechanistically, Mig-BCBM harbored ATF6, a critical transducer of endoplasmic reticulum (ER) stress. Upon internalization into hCMEC/D₃ cells, ATF6 elicited robust ER stress responses, culminating in downregulation of ZO-1 and VE-cadherin. Digital PCR analysis disclosed significant upregulation of ATF6 in serum migrasomes derived from BCBM patients compared to migrasomes from breast cancer patients and healthy individuals.</p><p><strong>Conclusions: </strong>This study uncovered a pivotal role of cancer cell-derived in BCBM by harnessing ATF6-mediated ER stress to disrupt the BBB and promote metastasis, suggesting novel diagnostic and therapeutic strategies targeting migrasomes and migrasome cargo.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Malignant ascites enhance γδ T cell cytotoxicity toward ovarian cancer <i>via</i> chemokine-mediated recruitment.","authors":"Zhanqun Yang, Ying Liu, Mengzhu Zheng, Hui Li, Ruoyao Cui, Pan Wang, Tianhui He, Hongyan Guo, Yinglin Zhou, Jian Lin, Long Chen","doi":"10.20892/j.issn.2095-3941.2025.0072","DOIUrl":"https://doi.org/10.20892/j.issn.2095-3941.2025.0072","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear PHGDH regulates macrophage polarization through transcriptional repression of <i>GLUD1</i> and <i>GLS2</i> in breast cancer.","authors":"Pei Wang, Xin Du, Zhiren Han, Jiaxin Zhong, Jiayu Yuan, Lin Jiang, Beinan Han, Wenkui Fu, Hongde Li, Hai Hu, Zhenkun Na","doi":"10.20892/j.issn.2095-3941.2024.0398","DOIUrl":"10.20892/j.issn.2095-3941.2024.0398","url":null,"abstract":"<p><strong>Objective: </strong>Tumor-associated macrophages (TAMs) exhibit heterogeneous properties including anti-tumorigenic and pro-tumorigenic phenotypes. The rate-limiting enzyme in <i>de novo</i> serine biosynthesis, 3-phosphoglycerate dehydrogenase (PHGDH), has a well-established role in cellular metabolism, yet its specific role in macrophages remains unknown.</p><p><strong>Methods: </strong>Metabolomics assays were conducted to assess metabolite composition and dynamics in macrophages. Changes in polarization and immunosuppressive markers were validated with qRT-PCR. Bioinformatics was used to analyze immune cell subsets and associated metabolic pathways. Finally, ChIP-qPCR and co-immunoprecipitation assays were performed to elucidate the downstream regulatory mechanisms of PHGDH.</p><p><strong>Results: </strong>Serine metabolism was found to be downregulated in TAMs in breast cancer. Functional studies revealed that PHGDH inhibition promotes an M2-like phenotype and immunosuppressive functions in macrophages. Furthermore, PHGDH was found to undergo nuclear translocation during macrophage polarization. Mechanistically, nuclear PHGDH was found to regulate <i>GLUD1</i> and <i>GLS2</i> transcription <i>via</i> interaction with the transcription factor STAT3. Rescue experiments demonstrated that glutamine supplementation and STAT3 inhibition reversed the effects of PHGDH on macrophage function.</p><p><strong>Conclusions: </strong>Our findings reveal a previously unrecognized non-canonical metabolic function of PHGDH, thus providing potential therapeutic targets in the tumor microenvironment for reversing malignant progression.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in the treatment of metastatic prostate cancer in China.","authors":"Baojun Wang, Zhenhua Liu, Luyao Yang, Xu Zhang","doi":"10.20892/j.issn.2095-3941.2025.0065","DOIUrl":"10.20892/j.issn.2095-3941.2025.0065","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAR T-cell therapy for relapsed/refractory CD5-positive diffuse large B-cell lymphoma yields more favorable outcomes than standard therapy.","authors":"Hui Luo, Tongjuan Li, Fankai Meng, Zhenya Hong, Yang Cao, Gaoxiang Wang, Liang Huang, Xiaoxi Zhou","doi":"10.20892/j.issn.2095-3941.2024.0626","DOIUrl":"10.20892/j.issn.2095-3941.2024.0626","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senescent macrophages in cancer: roles in tumor progression and treatment opportunities.","authors":"Tianzi Wang, Chang Liu, Xuefeng Hu, Ning Yang, Chen Qiu","doi":"10.20892/j.issn.2095-3941.2024.0589","DOIUrl":"10.20892/j.issn.2095-3941.2024.0589","url":null,"abstract":"<p><p>Senescent macrophages have emerged as dynamic cells within the tumor microenvironment that significantly promote tumor progression through complex cellular and molecular functional alterations. This review explores the multifaceted roles of macrophage senescence in cancer, and establishes links between senescent macrophages and tumor progression from multiple perspectives, on the basis of the first comprehensive analysis of the molecular mechanisms and pathways involved. By systematically examining the diverse changes in senescent macrophages, this review integrates and analyzes their effects on tumors, thus offering a comprehensive and novel theoretical foundation, and practical insights for cancer treatment. Notably, by integrating current molecular research and therapeutic advancements, we summarize novel therapeutic strategies targeting senescent macrophages, including senolytics, senescence modulators, and cutting-edge immunotherapies, thereby highlighting the potential of senescent macrophages as a therapeutic target and introducing new opportunities for cancer treatment.</p>","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic value of peripheral eosinophil counts in patients with newly diagnosed multiple myeloma.","authors":"Xu Chen, Xiaoyan Yue, Hao Jiang, Qianqian Yang, Jinwen Huang, Wenjue Pan, Xiujie Zhao, Xiufeng Yin, Panpan Wang, Liangning Hu, Xiaoli Guo, Fangfei Shao, Haowen Xiao","doi":"10.20892/j.issn.2095-3941.2024.0448","DOIUrl":"10.20892/j.issn.2095-3941.2024.0448","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The evidence and concerns about screening ultrasound for breast cancer.","authors":"Huijiao Yan, Qiankun Wang, Fanghui Zhao, Daehee Kang, Youlin Qiao","doi":"10.20892/j.issn.2095-3941.2024.0562","DOIUrl":"10.20892/j.issn.2095-3941.2024.0562","url":null,"abstract":"","PeriodicalId":9611,"journal":{"name":"Cancer Biology & Medicine","volume":" ","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12032836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}