Cell Research最新文献

Bridging the gap: how sperm’s core structure explains male infertility 弥合鸿沟：精子的核心结构如何解释男性不育

IF 44.1 1区生物学

Cell Research Pub Date : 2025-07-15 DOI: 10.1038/s41422-025-01150-3

Thibault Legal, Khanh Huy Bui

引用次数: 0

Human myelocyte and metamyelocyte-stage neutrophils suppress tumor immunity and promote cancer progression 人髓细胞和偏髓细胞期中性粒细胞抑制肿瘤免疫并促进癌症进展

IF 44.1 1区生物学

Cell Research Pub Date : 2025-07-15 DOI: 10.1038/s41422-025-01145-0

Wei Liu, Tao Shi, Chun Lu, Keying Che, Zijian Zhang, Yuting Luo, Daniel Hirschhorn, Hanbing Wang, Shaorui Liu, Yan Wang, Shuang Liu, Haiqiao Sun, Jun Lu, Yuan Liu, Dongquan Shi, Shuai Ding, Heping Xu, Liaoxun Lu, Jianming Xu, Jun Xin, Yinming Liang, Taha Merghoub, Jia Wei, Yan Li

{"title":"Human myelocyte and metamyelocyte-stage neutrophils suppress tumor immunity and promote cancer progression","authors":"Wei Liu, Tao Shi, Chun Lu, Keying Che, Zijian Zhang, Yuting Luo, Daniel Hirschhorn, Hanbing Wang, Shaorui Liu, Yan Wang, Shuang Liu, Haiqiao Sun, Jun Lu, Yuan Liu, Dongquan Shi, Shuai Ding, Heping Xu, Liaoxun Lu, Jianming Xu, Jun Xin, Yinming Liang, Taha Merghoub, Jia Wei, Yan Li","doi":"10.1038/s41422-025-01145-0","DOIUrl":"https://doi.org/10.1038/s41422-025-01145-0","url":null,"abstract":"Tumor-infiltrating neutrophils (TINs) are highly heterogeneous and mostly immunosuppressive in the tumor immune microenvironment (TIME). Current biomarkers of TINs and treatment strategies targeting TINs have not yielded optimal responses in patients across cancer types. Here, we separated human and mouse neutrophils into three developmental stages, including promyelocyte (PM), myelocyte & metamyelocyte (MC & MM), and band & segmented (BD & SC) neutrophils. Based on this separation, we observed the predominance of human but not mouse MC & MM-stage neutrophils in bone marrow (BM), which exhibit potent immunosuppressive and tumor-promoting properties. MCs & MMs also occupy the majority of TINs among patients with 17 cancer types. Moreover, through the creation of a NOD/ShiLtJGpt-Prkdcem26Cd52Il2rgem26Cd22/Gpt (NCG)-Gfi1−/− human immune system (HIS) mouse model, which supports efficient reconstitution of human TIN, we found a significant increase of BM MCs & MMs in tumor-bearing mice. By comparing the single-cell RNA sequencing analysis results of human neutrophils from both BM and tumors, we found that CD63 and Galectin-3 distinguish MC & MM from neutrophil populations in cancer patients. Furthermore, we proposed a strategy with Fms-like tyrosine kinase 3 ligand to specifically induce the trans-differentiation of MCs & MMs into monocytic cells, and trigger tumor control in NCG-Gfi1−/− HIS mice. Thus, our findings establish an essential role of human MC & MM-stage neutrophils in promoting cancer progression, and suggest their potential as targets for developing potential biomarkers and immunotherapies for cancer.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"22 1","pages":""},"PeriodicalIF":44.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Too sweet to be savory: how fructose elicits microglia-driven disturbance of neurodevelopment 甜到不能入味：果糖如何引起小胶质细胞驱动的神经发育障碍

IF 44.1 1区生物学

Cell Research Pub Date : 2025-07-15 DOI: 10.1038/s41422-025-01148-x

Maximilian Fliegauf, Marco Prinz

引用次数: 0

Organelle biology: emerging themes and future directions. 细胞器生物学：新兴主题和未来方向。

IF 28.1 1区生物学

Cell Research Pub Date : 2025-07-11 DOI: 10.1038/s41422-025-01147-y

Shulin Li, Liang Ge

引用次数: 0

Author Correction: Dual-specificity histone demethylase KIAA1718 (KDM7A) regulates neural differentiation through FGF4 作者更正：双特异性组蛋白去甲基酶KIAA1718 （KDM7A）通过FGF4调节神经分化

IF 44.1 1区生物学

Cell Research Pub Date : 2025-07-10 DOI: 10.1038/s41422-025-01143-2

Chengyang Huang, Yang Xiang, Yanru Wang, Xia Li, Longyong Xu, Ziqi Zhu, Ting Zhang, Qingqing Zhu, Kejing Zhang, Naihe Jing, Charlie Degui Chen

引用次数: 0

Escaping ageing through Cell Annealing—a phenomenological model 通过细胞退火来逃避衰老——一个现象学模型

IF 44.1 1区生物学

Cell Research Pub Date : 2025-07-08 DOI: 10.1038/s41422-025-01138-z

Sebastian Memczak, Juan Carlos Izpisua Belmonte, Thore Graepel

引用次数: 0

A patient-derived organoid model captures fetal-like plasticity in colorectal cancer. 患者来源的类器官模型捕获结肠直肠癌胎儿样可塑性。

IF 28.1 1区生物学

Cell Research Pub Date : 2025-07-04 DOI: 10.1038/s41422-025-01139-y

Liang Xiong, Ying Xu, Zhaoya Gao, Jingyi Shi, Yunfan Wang, Xiaodong Wang, Wensheng Huang, Ming Li, Longteng Wang, Jun Xu, Cheng Li, Jin Gu, Hongkui Deng, Molong Qu

{"title":"A patient-derived organoid model captures fetal-like plasticity in colorectal cancer.","authors":"Liang Xiong, Ying Xu, Zhaoya Gao, Jingyi Shi, Yunfan Wang, Xiaodong Wang, Wensheng Huang, Ming Li, Longteng Wang, Jun Xu, Cheng Li, Jin Gu, Hongkui Deng, Molong Qu","doi":"10.1038/s41422-025-01139-y","DOIUrl":"10.1038/s41422-025-01139-y","url":null,"abstract":"Phenotypic plasticity is a hallmark feature driving cancer progression, metastasis, and therapy resistance. Fetal-like transcriptional programs have been increasingly implicated in promoting plastic cell states, yet their roles remain difficult to study due to limitations of existing culture models. Here, we establish a chemically defined patient-derived organoid system that enables long-term expansion of colorectal cancer (CRC) cells while preserving fetal-like features associated with phenotypic plasticity. Using this model, we identify an oncofetal state (OnFS) that is enriched in advanced tumors and linked to key features of plasticity, including epithelial-mesenchymal plasticity, as well as increased metastasis and treatment resistance. Mechanistically, we show that FGF2-AP-1 signaling maintains the OnFS program and associated phenotypic plasticity in CRC. This model offers a powerful platform for studying the fetal-like features underlying cancer cell plasticity and their role in tumor progression and treatment resistance in CRC.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":" ","pages":""},"PeriodicalIF":28.1,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144564631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differentiation therapy with hepatocyte nuclear factor 4α for patients with hepatocellular carcinoma. 肝细胞核因子4α对肝癌患者的分化治疗。

IF 28.1 1区生物学

Cell Research Pub Date : 2025-07-04 DOI: 10.1038/s41422-025-01142-3

Chuan Yin, Wen-Ping Xu, Wei-Hua Dong, Chen-Hong Ding, Jia-Rong Cai, Xin Zeng, Si-Han Wu, Pei-Mei Shi, Xin Zhang, Wei-Fen Xie

引用次数: 0

Phrixotoxin-3 binds to three distinct antagonistic sites on human Na_v1.6. Phrixotoxin-3结合到人类Nav1.6上的三个不同的拮抗位点。

IF 28.1 1区生物学

Cell Research Pub Date : 2025-07-04 DOI: 10.1038/s41422-025-01141-4

Xiao Fan, Jiaofeng Chen, Xiaoshuang Huang, Zhanfeng Hou, Yuzhen Xie, Zigang Li, Nieng Yan, Jian Huang

引用次数: 0

Deubiquitinase-dependent transcriptional silencing controls inflammation 去泛素酶依赖的转录沉默控制炎症

IF 44.1 1区生物学

Cell Research Pub Date : 2025-07-03 DOI: 10.1038/s41422-025-01140-5

Yuxin Yi, Wenjie Xu, Pengcheng Mi, Siliang Ye, Li Chen, Neal M. Alto, Zixu Liu

{"title":"Deubiquitinase-dependent transcriptional silencing controls inflammation","authors":"Yuxin Yi, Wenjie Xu, Pengcheng Mi, Siliang Ye, Li Chen, Neal M. Alto, Zixu Liu","doi":"10.1038/s41422-025-01140-5","DOIUrl":"https://doi.org/10.1038/s41422-025-01140-5","url":null,"abstract":"Transcriptional control is crucial for the regulation of inflammation. While it is well-established that inducible transcriptional repressors are synthesized de novo through signal-dependent transcriptional upregulation, it remains unclear whether post-translational modification mechanisms, such as deubiquitination, also contribute to this process. We previously identified developmentally silenced sine oculis (SIX) transcription factors that are reactivated to control inflammatory gene transcription in differentiated immune cells under chronic microbial infections. However, the molecular mechanisms by which this transcriptional silencing process is regulated remain unclear. Here, we report that USP2, a deubiquitinase localized in the nucleus and induced by inflammatory signals, stabilizes SIX proteins through deubiquitination under inflammatory conditions. Consequently, the USP2-SIX complex acts in concert to control NF-κB-mediated inflammatory gene transcription by directly targeting gene promoters. Supporting this mechanism, Usp2−/− mice exhibit higher mortality during H1N1 infections, which phenocopies Six1−/− mice, attributed to elevated levels of life-threatening inflammatory mediators and exacerbated pathology. This study establishes a deubiquitinase-dependent transcriptional control of the inflammatory response to prevent immunopathology, offering new therapeutic avenues for combating infectious diseases.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"70 1 1","pages":""},"PeriodicalIF":44.1,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144547107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0