Cancer letters最新文献_第9页

Targeting p53 for immune modulation: Exploring its functions in tumor immunity and inflammation 靶向p53的免疫调节：探讨其在肿瘤免疫和炎症中的功能。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-03-05 DOI: 10.1016/j.canlet.2025.217614

H. Helena Wu , Sarah Leng , David D. Eisenstat , Consolato Sergi , Roger Leng

{"title":"Targeting p53 for immune modulation: Exploring its functions in tumor immunity and inflammation","authors":"H. Helena Wu , Sarah Leng , David D. Eisenstat , Consolato Sergi , Roger Leng","doi":"10.1016/j.canlet.2025.217614","DOIUrl":"10.1016/j.canlet.2025.217614","url":null,"abstract":"<div><div>p53, often referred to as the “guardian of the genome,” is a critical regulator of cellular responses to stress. p53 plays a dual role in tumor suppression and immune regulation. In addition to its well-known functions of maintaining genomic stability and inducing apoptosis, p53 orchestrates a complex interaction between innate and adaptive immune responses. This involvement contributes to pathogen clearance, immune surveillance, and immunogenic cell death (ICD). This review explores the influence of p53 on immune dynamics, detailing its effects on macrophages, dendritic cells, natural killer cells (NK), T cells, and B cells. This review explains how mutations in p53 disrupt immune responses, promoting tumor immune evasion, and highlights its regulation of inflammatory cytokines and pattern recognition receptors. Furthermore, p53's role in ICD marks it as a key player in antitumor immunity, which has significant implications for cancer immunotherapy. The review also discusses the role of p53 in inflammation, autoimmune diseases, and chronic infections, revealing its dual function in promoting and suppressing inflammation through interactions with NF-κB signaling. Therapeutically, approaches that target p53, including wild-type p53 reactivation and combination therapies with immune checkpoint inhibitors, show considerable promise. Advances in high-throughput technologies, such as single-cell RNA sequencing and CRISPR screens, provide new insights into the immunological functions of p53, including its role in microbiome-immune interactions and immune senescence. This comprehensive review highlights the importance of incorporating immunological insights from p53 into innovative therapeutic strategies, addressing existing knowledge gaps, and paving the way for personalized medicine.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"617 ","pages":"Article 217614"},"PeriodicalIF":9.1,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SF3B4-mediated alternative splicing in cancer development and progression sf3b4介导的选择性剪接在癌症发生和进展中的作用。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-03-04 DOI: 10.1016/j.canlet.2025.217597

Hanqi Zhang , Pangzhou Chen , Zhi Tian , Hailin Tang , Ziyun Guan , Yutian Zou

引用次数: 0

Corrigendum to “KIAA1429 facilitates metastasis via m6A-YTHDC1-dependent RND3 down-regulation in hepatocellular carcinoma cells” [Canc. Lett. 584 (2024) 216598] “KIAA1429通过肝癌细胞中m6a - ythdc1依赖性RND3下调促进转移”的更正[Canc。Lett. 584(2024) 216598]。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-03-04 DOI: 10.1016/j.canlet.2025.217593

Meihua Shan , Dong Liu , Liangbo Sun , Mingzhen Yang , Meng He , Yang Zhang , Li Xiang , Haiyan He , Dun Niu , Lingxi Chen , Shuhui Li , An Chen , Fengtian He , Yue Wang , Jiqin Lian

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Advancing glioblastoma therapy: Learning from the past and innovations for the future 推进胶质母细胞瘤治疗：从过去的学习和未来的创新。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-03-02 DOI: 10.1016/j.canlet.2025.217601

Mandeep Rana , Ke-Chi Liou , Amandeep Thakur , Kunal Nepali , Jing-Ping Liou

{"title":"Advancing glioblastoma therapy: Learning from the past and innovations for the future","authors":"Mandeep Rana , Ke-Chi Liou , Amandeep Thakur , Kunal Nepali , Jing-Ping Liou","doi":"10.1016/j.canlet.2025.217601","DOIUrl":"10.1016/j.canlet.2025.217601","url":null,"abstract":"<div><div>Marred by a median survival of only around 12–15 months coupled with poor prognosis and effective therapeutic deprived drug armory, treatment/management of glioblastoma has proved to be a daunting task. Surgical resection, flanked by radiotherapy and chemotherapy with temozolomide, stands as the standard of care; however, this trimodal therapy often manifests limited efficacy due to the heterogeneous and highly infiltrative nature of GBM cells. In addition, the existence of the blood-brain barrier, tumor microenvironment, and the immunosuppressive nature of GBM, along with the encountered resistance of GBM cells towards conventional therapy, also hinders the therapeutic applications of chemotherapeutics in GBM. This review presents key insights into the molecular pathology of GBM, including genetic mutations, signaling pathways, and tumor microenvironment characteristics. Recent innovations such as immunotherapy, oncolytic viral therapies, vaccines, nanotechnology, electric field, and cancer neuroscience, as well as their clinical progress, have been covered. In addition, this compilation also encompasses a discussion on the role of personalized medicine in tailoring treatments based on individual tumor profiles, an approach that is gradually shifting the paradigm in GBM management. Endowed with the learnings imbibed from past failures coupled with the zeal to embrace novel/multidisciplinary approaches, researchers appear to be on the right track to pinpoint more effective and durable solutions in the context of GBM treatment.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"617 ","pages":"Article 217601"},"PeriodicalIF":9.1,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PARP1 in melanoma: Mechanistic insights and implications for basic and clinical research PARP1在黑色素瘤中的作用：基础和临床研究的机制见解和意义。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-02-28 DOI: 10.1016/j.canlet.2025.217599

Andrea Marranci , Luisa Maresca , Samuele Lodovichi , Andrea Ghelli Luserna di Rorà , Barbara Stecca , Laura Poliseno

{"title":"PARP1 in melanoma: Mechanistic insights and implications for basic and clinical research","authors":"Andrea Marranci , Luisa Maresca , Samuele Lodovichi , Andrea Ghelli Luserna di Rorà , Barbara Stecca , Laura Poliseno","doi":"10.1016/j.canlet.2025.217599","DOIUrl":"10.1016/j.canlet.2025.217599","url":null,"abstract":"<div><div>Targeted therapies and immunotherapies have revolutionized the treatment of metastatic melanoma and have set a successful example for the treatment of other cancers. A similar breakthrough was achieved with the advent of PARP inhibitors (PARPi) in breast and ovarian cancer.</div><div>Recent evidence highlights the critical role of PARP1 in melanoma initiation and progression. High PARP1 expression correlates with aggressive melanoma characteristics and poor patient outcomes. Preclinical and clinical data suggest that PARPi, alone or in combination, can effectively reduce melanoma cell viability and inhibit tumor growth. However, integrating PARPi with current treatment approaches and identifying patients who could benefit the most from such combinations remain underexplored areas of investigation.</div><div>This review highlights the need for further basic and clinical research on PARP1 in melanoma, to better understand its role and to tackle major challenges in the field, such as resistance to targeted therapies and immune checkpoint inhibitors.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"617 ","pages":"Article 217599"},"PeriodicalIF":9.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Characterization of novel mouse esophageal squamous cell carcinoma cell lines and their utility as preclinical models 新型小鼠食管鳞状细胞癌细胞系的鉴定及其作为临床前模型的应用

IF 9.1 1区医学

Cancer letters Pub Date : 2025-02-28 DOI: 10.1016/j.canlet.2025.217600

Yang Li , Yuhao Wang , Guanzhu Ren , Hui Yu , Yin Yin , Lei Ma , Xiao Yu , Wangtianjiao Chen , Kai Zhang , Yahui Zhao , Zhihua liu

{"title":"Characterization of novel mouse esophageal squamous cell carcinoma cell lines and their utility as preclinical models","authors":"Yang Li , Yuhao Wang , Guanzhu Ren , Hui Yu , Yin Yin , Lei Ma , Xiao Yu , Wangtianjiao Chen , Kai Zhang , Yahui Zhao , Zhihua liu","doi":"10.1016/j.canlet.2025.217600","DOIUrl":"10.1016/j.canlet.2025.217600","url":null,"abstract":"<div><div>Esophageal squamous cell carcinoma (ESCC) has a high incidence, poor treatment response, and high mortality. Subcutaneous transplant tumor models are commonly used to study the immunosuppressive tumor microenvironment and its impact on immunotherapy. In this study, we established two new ESCC mouse cell lines, mEC525M and mEC586F, from 4NQO-induced ESCC mouse models of different sexes. We compared their proliferation, motility, and molecular characteristics with existing lines (HNM007, AKR, mEC25) using <em>in vitro</em> experiments and whole-exome sequencing. Treatment sensitivity analysis of all murine ESCC tumor cell lines revealed that AKR and HNM007 cells were more responsive to chemotherapy, mEC25 cells were more sensitive to radiotherapy, whereas mEC525M and mEC586F cells exhibited greater sensitivity to immunotherapy. Multiplex immunohistochemistry (mIHC) staining analysis revealed differences in immune infiltration among the tumors derived from the five mouse ESCC cell lines, with the highest proportion of T cells in mEC525M tumors, the highest proportion of CD11b<sup>+</sup> myeloid cells in mEC586F tumors and the highest proportion of CD19<sup>+</sup> B cells in mEC25 tumors. In addition, RNA sequencing results also revealed differences in immune responses exhibited by tumor tissues derived from the five mouse ESCC cell lines after anti-PD1 treatment. Therefore, this study offers a valuable tool for investigating the immune microenvironment in ESCC and supports the selection of mouse models for preclinical ESCC research.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"616 ","pages":"Article 217600"},"PeriodicalIF":9.1,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA HITT inhibits autophagy by attenuating ATG12-ATG5-ATG16L1 complex formation LncRNA HITT通过抑制ATG12-ATG5-ATG16L1复合物的形成来抑制自噬。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-02-27 DOI: 10.1016/j.canlet.2025.217532

Hao Liu , Xingwen Wang , Bolun Li , Zhiyuan Xiang , Yanan Zhao , Minqiao Lu , Qingyu Lin , Shanliang Zheng , Tianqi Guan , Yihong Zhang , Ying Hu

{"title":"LncRNA HITT inhibits autophagy by attenuating ATG12-ATG5-ATG16L1 complex formation","authors":"Hao Liu , Xingwen Wang , Bolun Li , Zhiyuan Xiang , Yanan Zhao , Minqiao Lu , Qingyu Lin , Shanliang Zheng , Tianqi Guan , Yihong Zhang , Ying Hu","doi":"10.1016/j.canlet.2025.217532","DOIUrl":"10.1016/j.canlet.2025.217532","url":null,"abstract":"<div><div>Dysregulated autophagy has been implicated in the pathogenesis of numerous diseases, including cancer. Despite extensive research on the underlying mechanisms of autophagy, the involvement of long non-coding RNAs (lncRNAs) remains poorly understood. Here, we demonstrate that a previously identified lncRNA, <em>HITT</em> (HIF-1α inhibitor at the translation level), is closely associated with biological processes such as autophagy through unbiased bioinformatic analysis. Subsequent studies demonstrate that <em>HITT</em> is increased by several autophagic stimuli, including PI-103, a potent inhibitor of PI3K and mTOR. This is caused by a reduction in the binding between <em>HITT</em> and AGO2, resulting in a reduction in the activity of <em>miR-205</em> towards HITT degradation. Increased <em>HITT</em> then binds to a key autophagy protein, Autophagy-related 5 (ATG5), and inhibits autophagosome formation by preventing the formation of the ATG12-ATG5-ATG16L1 complex. This results in <em>HITT</em> sensitizing PI-103-mediated cell death both <em>in vitro</em> and <em>in vivo</em> in nude mice by attenuating protective autophagy. The data presented herein demonstrate that <em>HITT</em> is a newly identified RNA regulator of autophagy and that it can be used to sensitize the colon cancer response to cell death by blocking the protective autophagy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"616 ","pages":"Article 217532"},"PeriodicalIF":9.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dietary intake of the red meat-derived glycan Neu5Gc fuels colorectal cancer through up-regulation of Wnt signaling pathway 膳食摄入红肉衍生聚糖Neu5Gc可通过上调Wnt信号通路促进结直肠癌的发生。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-02-27 DOI: 10.1016/j.canlet.2025.217598

Ana Luiza Lopes , Amanda Carlos Paulino , Mariana A.S. Thaumaturgo , Wallace Martins Araújo , Philippe Caloba , Kunio Kawanishi , Karl Willert , Rodrigo P. De Oliveira , João C. Machado , Felipe Lemos , Nissi Varki , Jose Andres Morgado-Diaz , Heinz Läubli , Adriane Regina Todeschini , Ajit Varki , Frederico Alisson-Silva

{"title":"Dietary intake of the red meat-derived glycan Neu5Gc fuels colorectal cancer through up-regulation of Wnt signaling pathway","authors":"Ana Luiza Lopes , Amanda Carlos Paulino , Mariana A.S. Thaumaturgo , Wallace Martins Araújo , Philippe Caloba , Kunio Kawanishi , Karl Willert , Rodrigo P. De Oliveira , João C. Machado , Felipe Lemos , Nissi Varki , Jose Andres Morgado-Diaz , Heinz Läubli , Adriane Regina Todeschini , Ajit Varki , Frederico Alisson-Silva","doi":"10.1016/j.canlet.2025.217598","DOIUrl":"10.1016/j.canlet.2025.217598","url":null,"abstract":"<div><div>Colorectal cancer (CRC) is a significant health concern, often linked to western diets, particularly red meat consumption. Several mechanisms, such as the high heme iron content, the formation of N-nitroso compounds (NOCs), heterocyclic amines (HCAs), and polycyclic aromatic hydrocarbons (PAHs), have been suggested to explain red meat's cancer-promoting effects. However, these factors are also found in fish and poultry, which are not linked to CRC risk. A new hypothesis attributes red meat's impact on CRC to its high content of a nonhuman glycan. While most mammals express N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc), humans express only Neu5Ac due to the loss of the CMAH enzyme. A red meat-rich diet leads to the incorporation of Neu5Gc into human cells, triggering an antibody-mediated inflammatory process known as xenosialitis. This study shows that Neu5Gc incorporation into CRC cells activates the Wnt/β-catenin signaling pathway, promoting cell proliferation. In a murine model lacking CMAH, a Neu5Gc-enriched diet induced intestinal polyp growth, with more malignant characteristics. Additionally, Neu5Gc incorporation in intestinal cells increased the expression of genes downstream of Wnt signaling. These findings reveal, for the first time in an <em>in vivo</em> model, a mechanism independent of immune response, where red meat consumption accelerates tumor progression through Neu5Gc incorporation. This activation of the Wnt/β-catenin signaling pathway provides new insight into how red meat consumption may influence CRC progression.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"616 ","pages":"Article 217598"},"PeriodicalIF":9.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic modification and tumor immunity: Unraveling the interplay with the tumor microenvironment and its therapeutic vulnerability and implications 表观遗传修饰和肿瘤免疫：揭示与肿瘤微环境的相互作用及其治疗脆弱性和意义。

IF 9.1 1区医学

Cancer letters Pub Date : 2025-02-27 DOI: 10.1016/j.canlet.2025.217587

Huaijin Zheng , Yuze Hua , Sen Yang , Vincent Liu , Nan Huang , Jiayi Li , Jorg Kleeff , Quan Liao , Qiaofei Liu

{"title":"Epigenetic modification and tumor immunity: Unraveling the interplay with the tumor microenvironment and its therapeutic vulnerability and implications","authors":"Huaijin Zheng , Yuze Hua , Sen Yang , Vincent Liu , Nan Huang , Jiayi Li , Jorg Kleeff , Quan Liao , Qiaofei Liu","doi":"10.1016/j.canlet.2025.217587","DOIUrl":"10.1016/j.canlet.2025.217587","url":null,"abstract":"<div><div>In the ever-evolving arena of molecular biology, epigenetic modifications stand out as crucial determinants in the orchestration of cellular identity, function, and fate. This review analyzes the close relationship between epigenetics and tumor immunity, emphasizing the intricate interplay with the tumor microenvironment (TME). Rooted in the knowledge that the incidence of cancer correlates strongly with the biological and genetic age, we highlight DNA methylation as a cornerstone of the “epigenetic aging” process with close ties to tumorigenesis. The TME, with its diverse cellular and acellular constituents, is an active participant in tumor biology, further complicated by epigenetic alterations. These modifications, from DNA methylation to histone changes, not only shape the TME but are reciprocally influenced by it, reinforcing a cycle that propels malignancy. Through this exploration, we underline the importance of understanding this mutual relationship, as it holds significant implications for tumor growth, heterogeneity, and therapeutic resistance. Ultimately, this review illuminates the potential of harnessing epigenetic insights for innovative cancer therapeutic strategies, pointing towards a promising avenue for future cancer management.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"616 ","pages":"Article 217587"},"PeriodicalIF":9.1,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Leukemia confers a durable imprint on healthy hematopoietic stem and progenitor cells 白血病会给健康的造血干细胞和祖细胞留下持久的印记

IF 9.1 1区医学

Cancer letters Pub Date : 2025-02-26 DOI: 10.1016/j.canlet.2025.217590

Ding-Wen Chen , Julie M. Schrey , Eric K. Wafula , Jian-Meng Fan , Sarah E. Adams , Deanne M. Taylor , Peter Kurre

{"title":"Leukemia confers a durable imprint on healthy hematopoietic stem and progenitor cells","authors":"Ding-Wen Chen , Julie M. Schrey , Eric K. Wafula , Jian-Meng Fan , Sarah E. Adams , Deanne M. Taylor , Peter Kurre","doi":"10.1016/j.canlet.2025.217590","DOIUrl":"10.1016/j.canlet.2025.217590","url":null,"abstract":"<div><div>Recent models of infection and experimental inflammation reveal that hematopoietic stem and progenitor cells (HSPCs) can generate a memory of the exposure. While the acute inflammatory activity rapidly resolves, cells acquire a heightened capacity to respond to subsequent stimulation. Inflammation is also a constitutive feature of cancer, including hematologic malignancies. Here, we adapt a translationally relevant model of acute myeloid leukemia (AML) to determine if inflammation in the bone marrow (BM) niche durably reprograms resident healthy HSPCs. To simulate the onset of malignancy and the subsequent remission, we generated hematopoietic chimera composed of healthy HSPCs and HSPCs bearing an inducible oncogenic human MLL-AF9 translocation expression cassette, a validated model of AML. Results show that the exposure to AML blasts in the BM leaves healthy HSPCs with transcriptomic changes and a shift to glycolytic metabolism during experimental remission. A secondary challenge of AML-experienced animals results in gene expression changes in inflammatory and metabolic pathways. These modified responses coincide with altered chromatin accessibility in AML-experienced HSPCs. Altogether, our observations provide first evidence for the durable inflammatory reprogramming of healthy HSPCs in the cancer microenvironment.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"616 ","pages":"Article 217590"},"PeriodicalIF":9.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0