Cell Death Discovery最新文献

{"title":"Transcription factor TCF3 promotes bladder cancer development via TMBIM6-Ca²⁺-dependent ferroptosis.","authors":"Wei-Feng Yang, Wei-Ming Guo, Qing-Tian Luo, Jingfen Lu, Zhou-Ke Tan, Yuan-Chun Ye, Gang Fan","doi":"10.1038/s41420-025-02585-8","DOIUrl":"10.1038/s41420-025-02585-8","url":null,"abstract":"<p><p>TMBIM6, a Ca²⁺ channel-like protein, shows an increased expression in numerous types of cancer. However, no study has reported its role in bladder cancer. This study aimed to explore the roles and mechanisms of TMBIM6 in bladder cancer. TMBIM6, ferroptosis-related proteins (GPX4, SLC7A11, and FTH1), and calmodulin (CaM) expressions in bladder cancer and paracancerous tissues were obtained by immunohistochemistry. The bladder cells were overexpressed or silenced with TCF3/TMBIM6 with ferroptosis inducer (Erastin)/Ca²⁺ blocker (BAPTA-AM) to investigate the effects on Ca²⁺-dependent ferroptosis and other functions. Finally, tumorigenicity was validated in nude mice. TMBIM6 and ferroptosis-related proteins were up-regulated in bladder cancer tissues, but CaM was downregulated. TMBIM6 overexpression enhanced proliferation, invasion, migration, GSH/GPX4 levels, and ferroptosis resistance while suppressing MDA, Fe²⁺, and lipid ROS in bladder cancer cells, effects reversed by Erastin. TCF3 was up-regulated in cancer and enriched in Ca²⁺ and ferroptosis-related pathways. TCF3 directly interacted with TMBIM6 and transcriptionally activated TMBIM6 expression. Both TCF3 and TMBIM6 overexpression exhibited comparable effects in modulating ferroptosis and other cellular processes, whereas TMBIM6 knockdown effectively reversed these phenotypic alterations. In addition, silencing TCF3 upregulated Ca²⁺ and CAM levels, while BAPTA-AM reversed these changes. In vivo, ov-TCF3 promoted tumor volume, weight, and TMBIM6 expression, and inhibited Ca²⁺ concentration, while Erastin reversed these changes. Our findings demonstrate that TCF3 facilitates bladder cancer progression through the enhancement of TMBIM6-Ca²⁺-mediated ferroptosis resistance. Both TCF3 and TMBIM6 emerge as promising biomarkers and therapeutic targets for bladder cancer intervention.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"303"},"PeriodicalIF":6.1,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding MUC1 and AR axis in a radiation-induced neuroendocrine prostate cancer cell-subpopulation unveils novel therapeutic targets.","authors":"Catarina Macedo-Silva, Ângela Albuquerque-Castro, Iris Carriço, Joana Lencart, Isa Carneiro, Lucia Altucci, João Lobo, Vera Miranda-Gonçalves, Rui Henrique, Margareta P Correia, Carmen Jerónimo","doi":"10.1038/s41420-025-02597-4","DOIUrl":"10.1038/s41420-025-02597-4","url":null,"abstract":"<p><p>Despite the initial efficacy of radiotherapy (RT) in treating prostate adenocarcinoma (PCa), disease progression can lead to the emergence of neuroendocrine prostate cancer (NEPC) - a highly aggressive malignancy for which standard therapies are mostly ineffective. Although oncogenic MUC1-C is a leading driver of NEPC and of PCa lineage plasticity, its putative role in response to RT, including RT-induced neuroendocrine transdifferentiation (tNED), has not been explored. We thus aimed to explore the interplay between androgen receptor (AR) signaling and MUC1 in PCa progression to NEPC. Firstly, using a radioresistant PCa cell line (22Rv1-RR), we demonstrated that epigenetic suppression of AR signaling led to MUC1/MUC1-C upregulation, which seems to be activated through γSTAT3. MUC1 activation is positively associated with increased expression of neuroendocrine-related markers, including CD56, chromogranin A, synaptophysin, and INSM transcriptional repressor 1 (INSM1). In NEPC tissues and compared to prostate adenocarcinoma, MUC1 was upregulated and negatively correlated with AR, which was suppressed. Finally, proteomic analyses revealed that MUC1 activation upon RT selective pressure led to the acquisition of stemness features, induction of epithelial to mesenchymal transition, and enhancement of basal cell-like traits. Notably, MUC1 knockdown significantly boosted response to RT in both 22Rv1-RR and DU145 cell lines. Moreover, AR-induced overexpression in PC3 cell lines entailed MUC1 downregulation, resulting in attenuated neuroendocrine traits and radioresistance, as well as impaired cell migration and invasion capabilities. Collectively, these results highlight MUC1 as a promising radiosensitization target and may ultimately help overcome therapy resistance and NEPC progression.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"306"},"PeriodicalIF":6.1,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyamines at the crossroad between cell metabolism and epigenetic regulation in acute leukemias.","authors":"Francesca Pirini, Anna Ferrari, Mouna Jandoubi, Irene Azzali, Davide Angeli, Rossana Mondrone, Chiara Bracci, Francesca Ruggieri, Giovanni Martinelli, Giorgia Simonetti","doi":"10.1038/s41420-025-02573-y","DOIUrl":"10.1038/s41420-025-02573-y","url":null,"abstract":"<p><p>Polyamines, namely putrescine, spermidine and spermine, are involved in multiple molecular pathways through their ability to bind nucleic acids and modulate protein stability. Their intracellular level is regulated through biosynthesis, catabolism and uptake from the extracellular milieu and the disruption of their homeostasis contributes to a variety of human disorders including cancer, as mainly described in solid tumors. Recently, there is an increasing interest in understanding polyamine functions in acute leukemias, due to the linkage between leukemic gene drivers, polyamine metabolism alterations and epigenetic defects. In particular, polyamine involvement in the regulation of acetylation and methylation is clinically relevant since epigenetic drugs are currently the backbone of novel therapeutic combinations, especially in acute myeloid leukemia (AML). With the exception of methylthioadenosine phosphorylase (MTAP), the enzyme leading to methionine regeneration that is frequently deleted in acute lymphoblastic leukemia (ALL), genes involved in polyamine metabolism and the interconnected methionine and arginine pathways are rarely targets of genetic lesions in acute leukemias. Conversely, functional alterations, including elevated polyamine levels and deregulated activity of enzymes involved in their metabolism, have been recently reported in leukemic cells. Notably, the polyamine catabolic enzyme spermidine/spermine N1 acetyltransferase (SAT1) that is overexpressed in AML and associated with a myeloproliferative phenotype, is a tumor suppressor gene in ALL, suggesting diverse mechanisms of action across hematological malignancies according to the lineage commitment and the differentiation stage. In light of the promising results achieved in AML and ALL by selective targeting of protein arginine methyltransferase 5 (PRMT5) and methionine adenosyltransferase 2A (MAT2A), two enzymes at the crossroad between polyamine metabolism and protein methylation, in this review we examine and discuss the role of polyamines in epigenetic regulation and other biological processes supporting leukemic cell survival, proliferation and differentiation, which provides the opportunity to discover additional polyamine-related targets and design novel therapeutic combinations.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"301"},"PeriodicalIF":6.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNMBP-AS1/hsa-miR-30a-5p/PGC1α axis suppresses tumor progression of colorectal cancer by inhibiting PKM2-mediated Warburg effect and enhance anti-PD-1 therapy efficacy.","authors":"Tianxiao Wang, Wenxin Zhang, Jiafeng Liu, Xiang Mao, Xinhai Wang, Jiyifan Li, Yuxin Huang, Zimei Wu, Haifei Chen, Huanying Shi, Huijie Qi, Lu Chen, Qunyi Li","doi":"10.1038/s41420-025-02561-2","DOIUrl":"10.1038/s41420-025-02561-2","url":null,"abstract":"<p><p>The Warburg effect, which is aerobic glycolysis, constitutes a major driver of various cancer progression. Therefore, we aimed to examine the role of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC1α) and its competing endogenous RNA (ceRNA) network in colorectal cancer (CRC) metabolic reprogramming. We used bioinformatics analysis and dual-luciferase reporter gene experiments and identified the DNMBP-AS1/hsa-miR-30a-5p/PGC1α ceRNA network. Additionally, we investigate the impact of PGC1α expression alterations on CRC proliferation and metabolic reprogramming. Moreover, we studied the influence of PGC1α on pyruvate kinase M2 (PKM2), and CRC malignant behavior manifestation. Our study has uncovered a significant association between the DNMBP-AS1/hsa-miR-30a-5p/PGC1α ceRNA network and CRC patient prognosis. Additionally, PGC1α overexpression impeded CRC growth, reduced glycolytic capacity, and enhanced anti-PD-1 therapy efficacy. PGC1α inhibited tumor cell glycolysis by downregulating the WNT/β-catenin pathway depending on peroxisome proliferator-activated receptor gamma (PPARγ), thereby suppressing PKM2. The PPARγ agonist rosiglitazone could hinder CRC proliferation and glycolytic activity. Combined with the PGC1α agonist ZLN005, it exhibits synergistic effects for treating CRC. Moreover, we verified that ZLN005 significantly potentiated PD-1 induced tumor suppression in xenograft mice. Finally, we demonstrated that PGC1α and PKM2 expression patterns in tumor tissues were closely related to patient prognosis. Moreover, we constructed a predictive model to predict the 5-year survival events in CRC patients using random forest model. Our results offer novel perspectives on the role of DNMBP-AS1/hsa-miR-30a-5p/PGC1α network in controlling CRC proliferation, metabolism and immune responses. Furthermore, our investigation reveals that using rosiglitazone combined with PGC1α agonist presents a promising therapeutic approach for managing CRC.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"299"},"PeriodicalIF":6.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-catenin safeguards cell survival via a transcription-independent mechanism during the induction of primitive streak from hESCs.","authors":"Peng Zhang, Xu-Xia Li, Hua-Jun Bai, Yongxu Zhao, Senle Rao, He Liang, Xiao-Ling Luo, Huang-Tian Yang","doi":"10.1038/s41420-025-02559-w","DOIUrl":"10.1038/s41420-025-02559-w","url":null,"abstract":"<p><p>The emergence of the primitive streak, representing an organizing center for gastrulation, marks the mesendodermal lineage specification from epiblast, in which the epiblast cells undergo highly organized collective behaviors to form mesendodermal cells properly. Cell death is observed at the peri-gastrulation stage, especially in the primitive streak region. However, the dynamic and regulatory mechanism of cell death in the primitive streak formation is unclear. Here, we observed that a quick inhibition of the fast elevated cell death is coinciding with an accumulation of β-catenin during the early stage of primitive streak induction from human embryonic stem cells (hESCs). Deficiency of β-catenin in hESCs does not affect their self-renewal but cause robust cell death after primitive streak induction, while neuroectodermal differentiation remains unchanged. Overexpression of full-length β-catenin in β-catenin-deficient hESCs restores the cell death restriction during induction of primitive streak. Mechanistically, the β-catenin-restricted cell death during primitive streak is transcription-independent. The accumulated β-catenin traps casein kinase-1 in β-catenin destruction complex following WNT activation via its ARM repeat domain, resulting in the inhibition of mTORC1 by stabilizing DEPTOR, subsequently attenuates mitochondrial translocation of p53 and enhances mitophagy to promote cell survival. Consistently, mTORC1 inhibition by rapamycin or RAD001 attenuates the cell death in β-catenin-deficient cells during induction of primitive streak. In addition, only the β-catenin retains activations of cell death restriction and transcriptional activity can promote hESCs to successfully differentiate into primitive streak and cardiomyocytes, suggesting that β-catenin-restricted cell death safeguards the fate transition during the primitive streak induction via offering a crucial window for the accumulation of β-catenin to induce lineage-specific genes. These findings provide new insights into the function and mechanisms by which β-catenin coordinates the cell death and early lineage commitment.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"300"},"PeriodicalIF":6.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyroptosis, a double-edged sword during pathogen infection: a review.","authors":"Yuanhang Zhang, Dengshuai Zhao, Tianyu Wang, Ping Li, Dixi Yu, Han Gao, Mengmeng Zhao, Limei Qin, Keshan Zhang","doi":"10.1038/s41420-025-02579-6","DOIUrl":"10.1038/s41420-025-02579-6","url":null,"abstract":"<p><p>Pyroptosis, a distinctive form of programmed cell death (PCD) characterized by its inflammatory nature, is triggered by the activation of pore-forming proteins known as gasdermins (GSDMs). This process is marked by progressive expansion of a pore within the cell, ultimately leading to cellular membrane disruption and the substantial release of intracellular contents. Pyroptosis plays a pivotal role in the eradication of intracellular pathogen replication niches and in the modulation of the immune system through the release of danger signals. Emerging evidence suggests that viruses have developed sophisticated strategies to evade immune surveillance and establish persistent infections by manipulating host pyroptotic pathway This review presents recent advances on the mechanisms by which two major pathogens (virus and bacteria) activate or inhibit the pyroptosis process through their effector proteins, thereby facilitating their dissemination and blocking host immunity. These insights provide new perspectives on the regulatory mechanisms of interactions between hosts and pathogens in the pyroptosis process.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"289"},"PeriodicalIF":6.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12217603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MCM9 deficiency impairs DNA damage repair during spermatogenesis, leading to Sertoli cell-only syndrome in humans.","authors":"Xuan Sha, Xin Zhang, Hao Geng, Yuqian Li, Xun Xia, Guotong Li, Rong Hua, Kuokuo Li, Yang Gao, Qunshan Shen, Rui Guo, Yuping Xu, Xiaojin He, Yunxia Cao, Mingxi Liu, Huan Wu","doi":"10.1038/s41420-025-02581-y","DOIUrl":"10.1038/s41420-025-02581-y","url":null,"abstract":"<p><p>Non-obstructive azoospermia (NOA) represents the most severe form of male infertility; however, its genetic etiology remains largely elusive. MCM9 is crucial for DNA damage repair in mammalian somatic cells, playing a key role in regulating both homologous recombination (HR) and mismatch repair (MMR) pathways. In mice, MCM9 deficiency leads to spermatogenic failure characterized by progressive germ cell depletion and impaired HR repair. However, the underlying mechanism remains unclear in humans. Our study identified two novel homozygous loss-of-function (LoF) mutations in MCM9 in two unrelated NOA patients presenting with Sertoli cell-only syndrome (SCOS). The absence of testicular MCM9 confirmed the pathogenicity of these LoF mutations. Furthermore, diminished HR-mediated DNA repair capacity observed in HEK293T cells, either lacking MCM9 or overexpressing mutant MCM9 plasmids, highlighted the deleterious impact of these LoF mutations on HR repair. Additionally, the confirmed interaction between human testicular MCM9 and both MSH2 and MLH1, alongside findings that human MCM9 is predominantly expressed in spermatogonial stem cells and spermatogonia, provides compelling evidence for the involvement of the MCM9-mediated MMR pathway in maintaining genomic integrity and supporting the viability and proliferation of spermatogonia in humans. Given the poor outcomes of microdissection testicular sperm extraction (micro-TESE) observed in both probands, we propose that biallelic LoF mutations in MCM9 may serve as non-invasive molecular biomarkers for predicting micro-TESE failure. These findings enhance our understanding of the genetic basis of human NOA, particularly SCOS, and provide valuable insights for genetic counseling and fertility guidance tailored to these patients.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"292"},"PeriodicalIF":6.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"N6-methyladenosine modification of MEF2A weakens cetuximab sensitivity in colorectal cancer via PD-L1/SOX12 axis.","authors":"Cao Gao, Jiajia He, Jiemin Zhao, Xuefeng Ni, Yanjie Xu","doi":"10.1038/s41420-025-02577-8","DOIUrl":"10.1038/s41420-025-02577-8","url":null,"abstract":"<p><p>Colorectal cancer (CRC) treatment is still a challenge due to chemoresistance. We explored MEF2A function and underlying mechanism on cetuximab sensitivity in CRC. In this study, cancer tissues and adjacent non-cancerous samples were harvested from CRC patients. Cell viability, proliferation and apoptosis in CRC cells were tested by CCK-8, EdU, colony formation, and flow cytometry assays. The binding of MEF2A on the PD-L1 promoter was validated using luciferase reporter assay, CHIP, and EMSA, while the relationship of PD-L1 and SOX12 mRNA, as well as RBM15/IGF2BP1 and MEF2A mRNA, was verified by RIP, RNA pull-down, or FISH combined with immunofluorescence. m6A modification level of MEF2A mRNA was assayed by MeRIP. The expressions of key genes and proteins, including MEF2A, PD-L1, SOX12, RBM15, IGF2BP1, apoptosis- and cell cycle-related proteins, were determined with RT-qPCR, western blot, or immunohistochemistry. In vivo function of MEF2A was validated by establishing a xenograft nude mice model. The results showed that MEF2A was increased in CRC cells and tissues, while it was higher in cetuximab-resistant CRC tissues. Silencing MEF2A improved the sensitivity of cetuximab in CRC cells and xenograft mice. MEF2A binds to PD-L1 promoter to transcriptionally upregulate PD-L1 expression. Increased cetuximab sensitivity was observed in PD-L1 knockout (KO) CRC cells. PD-L1 overexpression reversed the enhanced cetuximab sensitivity induced by MEF2A knockdown. PD-L1 binds to SOX12 mRNA to stabilize its expression. PD-L1 knockdown augmented cetuximab sensitivity, which was overturned by SOX12 overexpression. The m6A modification mediated by RBM15/IGF2BP1 upregulated MEF2A expression in cetuximab-resistant CRC tissues. In conclusion, m6A-modified MEF2A alleviated cetuximab sensitivity in CRC via PD-L1/SOX12 mRNA axis, indicating that MEF2A might function as a promising therapeutic target against cetuximab-resistant CRC.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"294"},"PeriodicalIF":6.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12219012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between genes and social environment: from epigenetics to precision medicine.","authors":"Sabrina Caporali, Simone Russo, Marcel Leist, Petra H Wirtz, Ivano Amelio","doi":"10.1038/s41420-025-02580-z","DOIUrl":"10.1038/s41420-025-02580-z","url":null,"abstract":"","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"293"},"PeriodicalIF":6.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Making sense of human colorectal cancer molecular subtypes: mice are stepping in.","authors":"Caleb Green, Pamela Roccia, Alessandro Rufini","doi":"10.1038/s41420-025-02594-7","DOIUrl":"10.1038/s41420-025-02594-7","url":null,"abstract":"","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"295"},"PeriodicalIF":6.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12216249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}