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Modern biology of extrachromosomal DNA: A decade-long voyage of discovery

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-03 DOI: 10.1038/s41422-024-01054-8

Qing-Lin Yang, Yipeng Xie, Kailiang Qiao, Jun Yi Stanley Lim, Sihan Wu

Genomic instability is a hallmark of cancer and is a major driving force of tumorigenesis. A key manifestation of genomic instability is the formation of extrachromosomal DNAs (ecDNAs) — acentric, circular DNA molecules ranging from 50 kb to 5 Mb in size, distinct from chromosomes. Ontological studies have revealed that ecDNA serves as a carrier of oncogenes, immunoregulatory genes, and enhancers, capable of driving elevated transcription of its cargo genes and cancer heterogeneity, leading to rapid tumor evolution and therapy resistance. Although ecDNA was documented over half a century ago, the past decade has witnessed a surge in breakthrough discoveries about its biological functions. Here, we systematically review the modern biology of ecDNA uncovered over the last ten years, focusing on how discoveries during this pioneering stage have illuminated our understanding of ecDNA-driven transcription, heterogeneity, and cancer progression. Furthermore, we discuss ongoing efforts to target ecDNA as a novel approach to cancer therapy. This burgeoning field is entering a new phase, poised to reshape our knowledge of cancer biology and therapeutic strategies.

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引用次数: 0

Neurotensin signaling in fat modulates food intake

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-03 DOI: 10.1038/s41422-024-01048-6

YoungUk Jang, Prashant Rajbhandari

White adipose tissue is a highly specialized organ that not only stores excess calories but also helps control systemic energy and glucose metabolism as an active endocrine organ. Fu et al.’s new study in Cell Research explains how secretory peptide neurotensin via interaction with its receptor in white adipocytes regulates food intake.

引用次数: 0

Donor MHC-specific thymus vaccination allows for immunocompatible allotransplantation

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-03 DOI: 10.1038/s41422-024-01049-5

Yang Liu, Hexi Feng, Ke Li, Ruiyi Li, Xiao-Jie Zhang, Ye Tian, Yujiang Fang, Yanjie Zhou, Ling Liu, Xiaoqing Zhang

Organ transplantation is the last-resort option to treat organ failure. However, less than 10% of patients benefit from this only option due to lack of major histocompatibility complex (MHC)-matched donor organs and 25%–80% of donated organs could not find MHC-matched recipients. T cell allorecognition is the principal mechanism for allogeneic graft rejection. We herein present a “donor MHC-specific thymus vaccination” (DMTV) strategy to induce T cell tolerance to both autologous and allogeneic donor MHC. Allogeneic MHC molecules were expressed in the recipient thymus through adeno-associated virus-mediated delivery, which led to stable expression of allogeneic MHC together with the autologous MHC in the engineered thymus. During local T cell education, those T cells recognizing either autologous MHC or allogeneic MHC were equally depleted. We constructed C57BL/6-MHC and BALB/c-MHC dual immunocompatible mice via thymus vaccination of C57BL/6-MHC into the BALB/c thymus and observed long-term graft tolerance after transplantation of C57BL/6 skin and C57BL/6 mouse embryonic stem cells into the vaccinated BALB/c mice. We also validated our DMTV strategy in a bone marrow, liver, thymus (BLT)-humanized mouse model for immunocompatible allotransplantation of human embryonic stem cells. Our study suggests that the DMTV strategy is a potent avenue to introduce a donor compatible immune system in recipients, which overcomes the clinical dilemma of the extreme shortage of MHC-matched donor organs for treating patients with end-stage organ failure.

{"title":"Donor MHC-specific thymus vaccination allows for immunocompatible allotransplantation","authors":"Yang Liu, Hexi Feng, Ke Li, Ruiyi Li, Xiao-Jie Zhang, Ye Tian, Yujiang Fang, Yanjie Zhou, Ling Liu, Xiaoqing Zhang","doi":"10.1038/s41422-024-01049-5","DOIUrl":"https://doi.org/10.1038/s41422-024-01049-5","url":null,"abstract":"<p>Organ transplantation is the last-resort option to treat organ failure. However, less than 10% of patients benefit from this only option due to lack of major histocompatibility complex (MHC)-matched donor organs and 25%–80% of donated organs could not find MHC-matched recipients. T cell allorecognition is the principal mechanism for allogeneic graft rejection. We herein present a “donor MHC-specific thymus vaccination” (DMTV) strategy to induce T cell tolerance to both autologous and allogeneic donor MHC. Allogeneic MHC molecules were expressed in the recipient thymus through adeno-associated virus-mediated delivery, which led to stable expression of allogeneic MHC together with the autologous MHC in the engineered thymus. During local T cell education, those T cells recognizing either autologous MHC or allogeneic MHC were equally depleted. We constructed C57BL/6-MHC and BALB/c-MHC dual immunocompatible mice via thymus vaccination of C57BL/6-MHC into the BALB/c thymus and observed long-term graft tolerance after transplantation of C57BL/6 skin and C57BL/6 mouse embryonic stem cells into the vaccinated BALB/c mice. We also validated our DMTV strategy in a bone marrow, liver, thymus (BLT)-humanized mouse model for immunocompatible allotransplantation of human embryonic stem cells. Our study suggests that the DMTV strategy is a potent avenue to introduce a donor compatible immune system in recipients, which overcomes the clinical dilemma of the extreme shortage of MHC-matched donor organs for treating patients with end-stage organ failure.</p>","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"34 1","pages":""},"PeriodicalIF":44.1,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142917019","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

LKB1 inactivation unleashes prostate cancer lineage plasticity

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-02 DOI: 10.1038/s41422-024-01030-2

Shaghayegh Nouruzi, Amina Zoubeidi

引用次数: 0

LKB1 inactivation promotes epigenetic remodeling-induced lineage plasticity and antiandrogen resistance in prostate cancer

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-02 DOI: 10.1038/s41422-024-01025-z

Fei Li, Pengfei Dai, Huili Shi, Yajuan Zhang, Juan He, Anuradha Gopalan, Dan Li, Yu Chen, Yarui Du, Guoliang Xu, Weiwei Yang, Chao Liang, Dong Gao

Epigenetic regulation profoundly influences the fate of cancer cells and their capacity to switch between lineages by modulating essential gene expression, thereby shaping tumor heterogeneity and therapy response. In castration-resistant prostate cancer (CRPC), the intricacies behind androgen receptor (AR)-independent lineage plasticity remain unclear, leading to a scarcity of effective clinical treatments. Utilizing single-cell RNA sequencing on both human and mouse prostate cancer samples, combined with whole-genome bisulfite sequencing and multiple genetically engineered mouse models, we investigated the molecular mechanism of AR-independent lineage plasticity and uncovered a potential therapeutic strategy. Single-cell transcriptomic profiling of human prostate cancers, both pre- and post-androgen deprivation therapy, revealed an association between liver kinase B1 (LKB1) pathway inactivation and AR independence. LKB1 inactivation led to AR-independent lineage plasticity and global DNA hypomethylation during prostate cancer progression. Importantly, the pharmacological inhibition of TET enzymes and supplementation with S-adenosyl methionine were found to effectively suppress AR-independent prostate cancer growth. These insights shed light on the mechanism driving AR-independent lineage plasticity and propose a potential therapeutic strategy by targeting DNA hypomethylation in AR-independent CRPC.

{"title":"LKB1 inactivation promotes epigenetic remodeling-induced lineage plasticity and antiandrogen resistance in prostate cancer","authors":"Fei Li, Pengfei Dai, Huili Shi, Yajuan Zhang, Juan He, Anuradha Gopalan, Dan Li, Yu Chen, Yarui Du, Guoliang Xu, Weiwei Yang, Chao Liang, Dong Gao","doi":"10.1038/s41422-024-01025-z","DOIUrl":"10.1038/s41422-024-01025-z","url":null,"abstract":"Epigenetic regulation profoundly influences the fate of cancer cells and their capacity to switch between lineages by modulating essential gene expression, thereby shaping tumor heterogeneity and therapy response. In castration-resistant prostate cancer (CRPC), the intricacies behind androgen receptor (AR)-independent lineage plasticity remain unclear, leading to a scarcity of effective clinical treatments. Utilizing single-cell RNA sequencing on both human and mouse prostate cancer samples, combined with whole-genome bisulfite sequencing and multiple genetically engineered mouse models, we investigated the molecular mechanism of AR-independent lineage plasticity and uncovered a potential therapeutic strategy. Single-cell transcriptomic profiling of human prostate cancers, both pre- and post-androgen deprivation therapy, revealed an association between liver kinase B1 (LKB1) pathway inactivation and AR independence. LKB1 inactivation led to AR-independent lineage plasticity and global DNA hypomethylation during prostate cancer progression. Importantly, the pharmacological inhibition of TET enzymes and supplementation with S-adenosyl methionine were found to effectively suppress AR-independent prostate cancer growth. These insights shed light on the mechanism driving AR-independent lineage plasticity and propose a potential therapeutic strategy by targeting DNA hypomethylation in AR-independent CRPC.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"35 1","pages":"59-71"},"PeriodicalIF":28.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41422-024-01025-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tau(t)ing glucocorticoid binding

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-02 DOI: 10.1038/s41422-024-01041-z

Sabine Vettorazzi, Jan Tuckermann

引用次数: 0

Reducing functionally defective old HSCs alleviates aging-related phenotypes in old recipient mice

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-02 DOI: 10.1038/s41422-024-01057-5

Yuting Wang, Wenhao Zhang, Chao Zhang, Hoang Q. Tran Van, Takashi Seino, Yi Zhang

Aging is a process accompanied by functional decline in tissues and organs with great social and medical consequences. Developing effective anti-aging strategies is of great significance. In this study, we demonstrated that transplantation of young hematopoietic stem cells (HSCs) into old mice can mitigate aging phenotypes, underscoring the crucial role of HSCs in the aging process. Through comprehensive molecular and functional analyses, we identified a subset of HSCs in aged mice that exhibit “younger” molecular profiles and functions, marked by low levels of CD150 expression. Mechanistically, CD150low HSCs from old mice but not their CD150high counterparts can effectively differentiate into downstream lineage cells. Notably, transplantation of old CD150low HSCs attenuates aging phenotypes and prolongs lifespan of elderly mice compared to those transplanted with unselected or CD150high HSCs. Importantly, reducing the dysfunctional CD150high HSCs can alleviate aging phenotypes in old recipient mice. Thus, our study demonstrates the presence of “younger” HSCs in old mice, and that aging-associated functional decline can be mitigated by reducing dysfunctional HSCs.

{"title":"Reducing functionally defective old HSCs alleviates aging-related phenotypes in old recipient mice","authors":"Yuting Wang, Wenhao Zhang, Chao Zhang, Hoang Q. Tran Van, Takashi Seino, Yi Zhang","doi":"10.1038/s41422-024-01057-5","DOIUrl":"10.1038/s41422-024-01057-5","url":null,"abstract":"Aging is a process accompanied by functional decline in tissues and organs with great social and medical consequences. Developing effective anti-aging strategies is of great significance. In this study, we demonstrated that transplantation of young hematopoietic stem cells (HSCs) into old mice can mitigate aging phenotypes, underscoring the crucial role of HSCs in the aging process. Through comprehensive molecular and functional analyses, we identified a subset of HSCs in aged mice that exhibit “younger” molecular profiles and functions, marked by low levels of CD150 expression. Mechanistically, CD150low HSCs from old mice but not their CD150high counterparts can effectively differentiate into downstream lineage cells. Notably, transplantation of old CD150low HSCs attenuates aging phenotypes and prolongs lifespan of elderly mice compared to those transplanted with unselected or CD150high HSCs. Importantly, reducing the dysfunctional CD150high HSCs can alleviate aging phenotypes in old recipient mice. Thus, our study demonstrates the presence of “younger” HSCs in old mice, and that aging-associated functional decline can be mitigated by reducing dysfunctional HSCs.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"35 1","pages":"45-58"},"PeriodicalIF":28.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41422-024-01057-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tau is a receptor with low affinity for glucocorticoids and is required for glucocorticoid-induced bone loss

IF 28.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2025-01-02 DOI: 10.1038/s41422-024-01016-0

Wenyu Fu, Meng Chen, Kaidi Wang, Yujianan Chen, Yazhou Cui, Yangli Xie, Zi-Ning Lei, Wenhuo Hu, Guodong Sun, Guiwu Huang, Chaopeng He, Jackie Fretz, Aubryanna Hettinghouse, Ronghan Liu, Xianyi Cai, Mingshuang Zhang, Yuehong Chen, Nan Jiang, Minchun He, Daniel H. Wiznia, Huiyun Xu, Zhe-Sheng Chen, Lin Chen, Kanglai Tang, Hong Zhou, Chuan-Ju Liu

Glucocorticoids (GCs) are the most prescribed anti-inflammatory and immunosuppressive drugs. However, their use is often limited by substantial side effects, such as GC-induced osteoporosis (GIO) with the underlying mechanisms still not fully understood. In this study, we identify Tau as a low-affinity binding receptor for GCs that plays a crucial role in GIO. Tau deficiency largely abolished bone loss induced by high-dose dexamethasone, a synthetic GC, in both inflammatory arthritis and GIO models. Furthermore, TRx0237, a Tau inhibitor identified from an FDA-approved drug library, effectively prevented GIO. Notably, combinatorial administration of TRx0237 and dexamethasone completely overcame the osteoporosis adverse effect of dexamethasone in treating inflammatory arthritis. These findings present Tau as a previously unrecognized GC receptor with low affinity, and provide potential strategies to mitigate a spectrum of GC-related adverse effects, particularly osteoporosis.

{"title":"Tau is a receptor with low affinity for glucocorticoids and is required for glucocorticoid-induced bone loss","authors":"Wenyu Fu, Meng Chen, Kaidi Wang, Yujianan Chen, Yazhou Cui, Yangli Xie, Zi-Ning Lei, Wenhuo Hu, Guodong Sun, Guiwu Huang, Chaopeng He, Jackie Fretz, Aubryanna Hettinghouse, Ronghan Liu, Xianyi Cai, Mingshuang Zhang, Yuehong Chen, Nan Jiang, Minchun He, Daniel H. Wiznia, Huiyun Xu, Zhe-Sheng Chen, Lin Chen, Kanglai Tang, Hong Zhou, Chuan-Ju Liu","doi":"10.1038/s41422-024-01016-0","DOIUrl":"10.1038/s41422-024-01016-0","url":null,"abstract":"Glucocorticoids (GCs) are the most prescribed anti-inflammatory and immunosuppressive drugs. However, their use is often limited by substantial side effects, such as GC-induced osteoporosis (GIO) with the underlying mechanisms still not fully understood. In this study, we identify Tau as a low-affinity binding receptor for GCs that plays a crucial role in GIO. Tau deficiency largely abolished bone loss induced by high-dose dexamethasone, a synthetic GC, in both inflammatory arthritis and GIO models. Furthermore, TRx0237, a Tau inhibitor identified from an FDA-approved drug library, effectively prevented GIO. Notably, combinatorial administration of TRx0237 and dexamethasone completely overcame the osteoporosis adverse effect of dexamethasone in treating inflammatory arthritis. These findings present Tau as a previously unrecognized GC receptor with low affinity, and provide potential strategies to mitigate a spectrum of GC-related adverse effects, particularly osteoporosis.","PeriodicalId":9926,"journal":{"name":"Cell Research","volume":"35 1","pages":"23-44"},"PeriodicalIF":28.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41422-024-01016-0.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142911556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Heat acclimation in mice requires preoptic BDNF neurons and postsynaptic potentiation

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-12-26 DOI: 10.1038/s41422-024-01064-6

Baoting Chen, Cuicui Gao, Changhao Liu, Tongtong Guo, Junwei Hu, Jialiang Xue, Kangmin Tang, Yuelai Chen, Tian Yu, Qiwei Shen, Hongbin Sun, Wen Z. Yang, Wei L. Shen

Dear Editor,

引用次数: 0

Astrocytes: emerging stars of engrams

IF 44.1 1区生物学 Q1 CELL BIOLOGY

Cell Research

Pub Date : 2024-12-23 DOI: 10.1038/s41422-024-01066-4

Sofiya Zbaranska, Sheena A. Josselyn

During learning experience, a subset of astrocytes in the hippocampus is activated and becomes both necessary and sufficient for subsequent memory recall. Williamson et al. discovered that these learning-associated astrocytes play an important role in memory by modulating engram neurons’ synaptic activity and facilitating the reactivation of engram neuron ensembles during memory retrieval.

引用次数: 0

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