Cell and Bioscience最新文献

{"title":"Key role of transcription factors network in proliferative vitreoretinal diseases development.","authors":"Clément Duveau, Yosra Raiss El Harrak, Azine Datlibagi, Jason Perret, François Willermain, Christine Delporte, Elie Motulsky","doi":"10.1186/s13578-026-01581-4","DOIUrl":"https://doi.org/10.1186/s13578-026-01581-4","url":null,"abstract":"<p><p>Proliferative vitreoretinal diseases (PVDs) encompass severe ocular disorders such as proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), and epiretinal membranes (ERM), characterized by the formation of fibrovascular membranes that often lead to retinal detachment and vision loss. A central mechanism driving these conditions is the epithelial-to-mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells, orchestrated by a network of transcription factors (TFs). Among these, zinc finger E-box binding homeobox 1 (ZEB1) emerges as a pivotal regulator by repressing epithelial markers like E-cadherin and inducing mesenchymal markers such as N-cadherin and vimentin, thereby promoting cell migration and fibrotic membrane formation. nuclear factor of activated T cells 5 (NFAT5) contributes to this process by mediating osmotic stress responses and upregulating inflammatory cytokines, which further act upon EMT and fibrosis. activator protein 1 (AP-1) and hypoxia inducible factor 1 subunit alpha (HIF-1α) participate in driving inflammation, extracellular matrix (ECM) remodeling, and angiogenesis. While HIF-1α triggers vascular endothelial growth factor (VEGF) expression under hypoxic conditions, AP-1 modulates matrix metalloproteinases (MMPs) essential for ECM degradation and remodeling. Additional TFs, including Kruppel-like factor 4 (KLF4) and microphthalmia-associated transcription factor (MITF), are vital in maintaining RPE cell identity. Their downregulation under pathological conditions disrupts epithelial integrity and predisposes cells to undergo EMT. Moreover, β-catenin, through its role in the wingless-related integration site (Wnt) signaling pathway, reinforces EMT and ECM remodeling, further enhancing fibrotic progression. Adipocyte enhancer-binding protein 1 (AEBP1) and ZFP36 ring finger protein like 1 (ZFP36L1) also regulate inflammatory responses and ECM dynamics, providing novel post-transcriptional targets for therapeutic intervention. Overall, the synergistic interactions among these TFs create complex feedback loops that amplify pathological changes in PVDs. Targeting these molecular pathways offers promising avenues for developing multi-targeted therapies aimed at saving vision-threatening disease while reducing invasive surgical interventions.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147857469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the 5-HT_1A receptor in the ventral hippocampus alleviates anxiety-like behavior in mice with angiotensin II-induced hypertension.","authors":"Wenjun Chen, Zhoucai Luo, Mingfeng Huang, Xiaoqi Zheng, Nating Xiong, Caiyan Gan, Jianlin Wu","doi":"10.1186/s13578-026-01583-2","DOIUrl":"https://doi.org/10.1186/s13578-026-01583-2","url":null,"abstract":"<p><p>Hypertension, a chronic condition, has affected > 1 billion people worldwide and is linked to a heightened risk of anxiety disorders. Despite this association, the exact mechanisms underlying the connections between hypertension and anxiety disorders remain largely elusive. In this research, we observed that systolic blood pressure (SBP) increased in mice subcutaneously administered with angiotensin II (Ang II) alongside signs of heightened anxiety. Furthermore, immunofluorescence and electrophysiological analyses revealed that Ang II enhanced neuronal activity and altered the synaptic activities of ventral CA1 (vCA1) neurons. Meanwhile, in vivo recordings showed that these neurons in Ang II-treated mice were significantly more responsive to anxiety-inducing stimuli. Additionally, chemogenetic inhibition of neural activity in vCA1 effectively alleviated anxiety-like behavior in the treated animal. Moreover, the expression of the serotonin receptor 5-HT_1A receptor (5-HT_1AR) in vCA1 was suppressed under hypertension. Activating these receptors with the agonist 8-OH-DPAT effectively modified neuronal excitability and reduced anxiety-related behavior in mice. These findings elucidate the critical role of vCA1 neural activity and 5-HT_1AR dysregulation in hypertension-associated anxiety, highlighting potential therapeutic targets for managing this condition.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147844955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cadmium impairs heart ventricular formation and disrupts polysialylated-NCAM/FGF receptor signaling in Xenopus tadpoles.","authors":"Pélagie Douchez, Ingrid Fliniaux, Yoshiko Takeda-Uchimura, Alain Martoriati, Matthieu Marin, Anne Harduin-Lepers, Katia Cailliau","doi":"10.1186/s13578-026-01579-y","DOIUrl":"https://doi.org/10.1186/s13578-026-01579-y","url":null,"abstract":"<p><strong>Background: </strong>Exposure to cadmium, a trace metallic element, is a major health concern. Cadmium is associated with a higher risk and predisposition to cardiovascular disease. Identifying molecular targets involved in such an effect is complexified by in utero embryonic and fetal development.</p><p><strong>Methods: </strong>To overcome those difficulties, we used the established vertebrate heart model of Xenopus laevis to analyze the neural cell adhesion molecules NCAM and FGF receptors involved in early cardiac development under cadmium treatment. Cadmium exposure is performed from fertilization until the completion of mature heart development at the end of stage 45. Additional molecular modifications occurring within the heart are detected in the expressing signaling system of Xenopus oocytes.</p><p><strong>Results: </strong>Exposure to cadmium results in the absence of heart ventricular myocardial trabeculae and disrupts the regulation of NCAM adhesion molecules and FGF receptor signaling in Xenopus. An increase in polysialylation (PSA) of NCAM is observed, accompanied by the deregulation in the expression of Golgi effectors Rab11 GTPase and Golph3. The sialyltransferases ST8Sia2 and ST8Sia4 are not increased at the transcriptional level but are accumulated in the Golgi apparatus. The highly sialylated NCAM interacts with the FGF receptor, prevents the formation of a complex with Integrin, FAK is O-GlcNAcylated, and the receptor translocation to the nucleus is impaired. Furthermore, the polysialylated-NCAM/FGF receptor signaling recruits higher amounts of Shp2 and leads to Erk2 hyperphosphorylation. Additionally, blocking FAK with a specific antibody in the normal polysialylated-NCAM/FGF receptor signaling causes the deregulated molecular phenotype.</p><p><strong>Conclusions: </strong>These results represent a significant advancement for future studies in environmental toxicology and cardiac developmental dysfunctions resulting from cadmium exposure.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147822171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of PTEN nuclear translocation by peptide Tat-K13 attenuates p-JUN-SESN2-AMPK-dependent autophagy and enhances neurological recovery after neonatal hypoxic-ischemic brain damage.","authors":"Chunfang Dai, Xiaobin Wu, Xiaohuan Li, Boqing Xu, Yayan Pang, Yunyun Huang, Xiangjun Dong, Nianrong Wang, Zhifang Dong","doi":"10.1186/s13578-026-01575-2","DOIUrl":"https://doi.org/10.1186/s13578-026-01575-2","url":null,"abstract":"<p><p>Neuronal death triggered by hypoxia-ischemia (HI) is a major cause of neonatal mortality and long-term neurological deficits. Excessive autophagy plays a pathogenic role in neonatal hypoxic-ischemic encephalopathy (HIE), and inhibition of phosphatase and tensin homolog deleted on chromosome TEN (PTEN) nuclear translocation has been shown to suppress autophagy. Our recent study demonstrated that blocking PTEN nuclear import with the peptide Tat-K13 mitigates HI-induced behavioral impairments. However, the underlying mechanism remains unclear. Here, we found that HI activated the p-JUN-SESN2-AMPK signaling pathway in both in vivo and in vitro models of neonatal hypoxic-ischemic brain damage (HIBD). Downregulation of JUN reduced neuronal loss and improved behavioral outcomes in HIBD rats. Furthermore, Tat-K13-mediated blockade of PTEN nuclear translocation attenuated HI-induced activation of the p-JUN-SESN2-AMPK pathway and suppressed autophagy. Notably, the neuroprotective and behavioral benefits conferred by Tat-K13 were achieved through autophagy inhibition resulting from suppression of this signaling cascade. These findings identify targeting PTEN nuclear import with Tat-K13 as a potential therapeutic strategy for neonatal HIE, acting via the p-JUN-SESN2-AMPK-autophagy axis to promote neuronal survival and functional recovery.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex.","authors":"Debin Xu, Jichun Yu, Yuting Yang, Yunyan Du, Hongcheng Lu, Shouhua Zhang, Qian Feng, Yi Yu, Liang Hao, Jun Shao, Leifeng Chen","doi":"10.1186/s13578-026-01560-9","DOIUrl":"10.1186/s13578-026-01560-9","url":null,"abstract":"","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":"16 1","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787051","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":"SIAH2-EPHB6 axis enhances filopodia formation in hepatocellular carcinoma cells by regulating RHOF.","authors":"Qinghe Hu, Kai Wu, Zhiyi Liu, Jiawei Xu, Weichao Yang, Nan Xia, Tianqi Hou, Yun Zhu, Kuan Cao, Hengliang Shi, Yi He, Bin Zhang","doi":"10.1186/s13578-026-01577-0","DOIUrl":"https://doi.org/10.1186/s13578-026-01577-0","url":null,"abstract":"<p><p>Seven in absentia homologue 2 (SIAH2) has been shown to contribute to the progression of various human tumors, including hepatocellular carcinoma (HCC). However, the precise mechanisms by which SIAH2 promotes HCC cell migration remain to be fully elucidated. In this study, we demonstrate that SIAH2 accelerates the invasion and migration of HCC cells by promoting K48-linked polyubiquitination and degradation of EPH receptor B6 (EPHB6). Notably, the invasion and migration of HCC cells regulated by the SIAH2-EPHB6 axis in association with enhanced filopodia formation, a critical early step in cell motility. Furthermore, our findings indicate that the SIAH2-EPHB6 axis promotes filopodia formation in HCC cells by modulating Ras homolog family member F (RHOF). Finally, we investigated the expression correlations among SIAH2, EPHB6, and RHOF using clinical tissue specimens. In summary, SIAH2 accelerates K48-linked polyubiquitination and degradation of EPHB6 to regulate filopodia formation in HCC cells.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Poly-GR promotes ferroptosis-associated vulnerability in C9orf72-ALS.","authors":"Chun-Yu Lin, Wen-Chi Hsieh, Shao-Ming Wang","doi":"10.1186/s13578-026-01574-3","DOIUrl":"https://doi.org/10.1186/s13578-026-01574-3","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent form of oxidative cell death driven by uncontrolled lipid peroxidation, has been increasingly implicated in neurodegeneration. However, its involvement and the underlying regulatory mechanism in C9orf72-linked amyotrophic lateral sclerosis (ALS), the most common genetic form of the disease, remain incompletely understood. Here, we show that the arginine-rich dipeptide repeat protein poly-GR promotes ferroptosis-associated molecular and biochemical features in motor neuron-like NSC34 cells. Poly-GR expression significantly increased lipid peroxidation, intracellular ferrous iron, and reactive oxygen species, indicating a cellular environment permissive for ferroptotic vulnerability. Mechanistically, poly-GR suppresses the Nrf2/Slc7a11 antioxidant defense axis by reducing Nrf2 nuclear localization and its occupancy at the Slc7a11 promoter, resulting in decreased Slc7a11 transcription. Restoration of Nrf2 or Slc7a11 expression attenuated lipid peroxidation and oxidative stress, while the iron chelator deferiprone effectively reduced Fe²⁺ accumulation and ferroptosis-associated injury. Functionally, poly-GR sensitized neuronal cells to erastin-induced ferroptotic stress-associated cell death, an effect reversed by Nrf2 or Slc7a11 overexpression and iron chelation. Together, these findings indicate that poly-GR disrupts redox homeostasis and iron metabolism to increase susceptibility to ferroptosis, highlighting the Nrf2/Slc7a11 pathway and labile iron regulation as potential therapeutic targets in C9orf72-associated ALS.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrator subunit IntS11 orchestrates the temporal dynamics of neural lineage progression in Drosophila.","authors":"Qiao Xiao, Liqiang Ai, Boquan Jia, Mengjia Kuang, Shengwei Xiao, Xiaoxue Bi, Yingbao Zhu, Guangxu Li, Wen Huang, Ranhui Duan","doi":"10.1186/s13578-026-01578-z","DOIUrl":"https://doi.org/10.1186/s13578-026-01578-z","url":null,"abstract":"<p><strong>Background: </strong>IntS11, the core catalytic subunit of the Integrator (INT), functions in various stages of transcription. However, its specific function in orchestrating neural lineage progression remains poorly understood.</p><p><strong>Results: </strong>Using a Drosophila model, we found that the absence of IntS11 leads to reduced brain size, which is not attributable to neuroblast (NB) loss or apoptosis but is due to impaired NB proliferation. MARCM (mosaic analysis with a repressible cell marker) revealed impaired clonal expansion, characterized by a significant decrease in progeny cell number. Live imaging and FUCCI analysis further confirmed a G1 arrest in IntS11-deficient NBs. Single-cell RNA-seq revealed downregulation of cell cycle regulators (aurB, CycE, Cdk4) in NBs and differentiation genes in GMCs, which were confirmed as candidates by ChIP-qPCR. Approximately 80% of neuronal morphogenesis-associated genes exhibiting 3'UTR shortening were downregulated. We further established that IntS11 physically binds to these loci to maintain lengthened 3'UTR isoforms and ensure mRNA stability in larval brains.</p><p><strong>Conclusions: </strong>Collectively, our findings establish IntS11 as a stage-specific regulator of neural lineage progression that sustains NB proliferation through transcriptional control of cell-cycle genes and stabilizes differentiation programs by maintaining long 3'UTR isoforms.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT5-RNF126 coordinated regulation of METTL17 stability controls mitochondrial function and glioma progression.","authors":"Chunyan He, Zixiao Zhang, Xiaoke Wu, Changjie Lin, Jieyu Jin, Yong Ni, Yingfeng Qian, Yin Wang","doi":"10.1186/s13578-026-01570-7","DOIUrl":"https://doi.org/10.1186/s13578-026-01570-7","url":null,"abstract":"<p><p>Gliomas are highly invasive brain tumors in which metabolic reprogramming plays a pivotal role in tumor initiation and progression. METTL17, a mitochondria-associated methyltransferase, has been reported to enhance oxidative phosphorylation (OXPHOS) through mitochondrial RNA methylation; however, its function and regulatory mechanisms in glioma remain poorly understood. In this study, we manipulated METTL17 expression in primary P1 and U251 glioma cells using lentiviral-mediated knockdown and overexpression approaches. METTL17 depletion significantly suppressed cell proliferation, migration, and invasion, reduced ATP production and mitochondrial membrane potential, and increased reactive oxygen species accumulation, whereas METTL17 overexpression reversed these phenotypes. Mechanistically, METTL17 sustained mitochondrial OXPHOS by positively regulating key components of the electron transport chain, including NDUFA2, NDUFS1, SDHB, UQCRB, and MT-CO2. Mass spectrometry and co-immunoprecipitation analyses further revealed that METTL17 interacts with the E3 ubiquitin ligase RNF126, which destabilizes METTL17 through K116-dependent ubiquitination. Additionally, we demonstrate that SIRT5 acts as a desuccinylase for METTL17, removing succinylation at Lys274 and thereby facilitating RNF126-mediated ubiquitination and degradation of METTL17. In vivo xenograft experiments further validated that METTL17 knockdown markedly inhibited tumor growth and enhanced apoptosis. Collectively, these findings identify METTL17 as a critical regulator of mitochondrial function and energy metabolism in glioma and reveal a SIRT5-METTL17-RNF126 axis that governs METTL17 stability, providing new insights into glioma metabolic reprogramming and potential therapeutic targets.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mouse model of HPV-associated cervicovaginal carcinosarcoma with comparative analysis to human clinical cases.","authors":"Jason Murray, Shiwen Peng, Chien-Fu Hung, T-C Wu, Deyin Xing","doi":"10.1186/s13578-026-01576-1","DOIUrl":"https://doi.org/10.1186/s13578-026-01576-1","url":null,"abstract":"<p><strong>Background: </strong>Carcinosarcomas of the gynecologic tract, previously referred to as malignant mixed müllerian/mesodermal tumor, are devastating malignancies that remain poorly studied due to their rarity and the lack of relevant model systems. Human papillomavirus (HPV)-associated carcinosarcomas are thought to arise from conventional HPV-driven squamous cell carcinomas or adenocarcinomas of the lower gynecologic tract, providing evidence to support the epithelial-to-mesenchymal transition (EMT) theory of carcinosarcoma tumorigenesis. Mouse models using HPV and oncogene plasmid cocktails to induce spontaneous squamous carcinomas have proven useful; however, they have not yet been applied to the study of carcinosarcomas or EMT.</p><p><strong>Results: </strong>Here, we describe a new series of eight human clinical cases of HPV-associated carcinosarcoma of the uterine cervix and vagina. To study this rare and aggressive disease, we applied an established HPV-driven mouse model under extended observation conditions, which resulted in the development of tumors with features of carcinosarcoma. We then characterized the resulting tumors with respect to histologic morphology, immunohistochemical profiles, and HPV expression patterns, demonstrating that the mouse tumors recapitulate key architectural patterns and diverse histomorphology of both the carcinomatous and sarcomatous components observed in human tumors. In addition, the mouse tumors exhibit immunohistochemical and HPV expression profiles similar to those seen in the clinical cases. In particular, detection of oncogenic high-risk HPV in both the carcinomatous and sarcomatous components of the human and mouse tumors provides evidence supporting an EMT-driven process with a shared etiology, although definitive mechanistic conclusions warrant further investigation.</p><p><strong>Conclusions: </strong>We present an extended characterization of an established HPV-driven in vivo model that, under prolonged observation, gives rise to carcinosarcoma-like tumors, a previously unrecognized phenomenon. Through comparative analysis with a newly described cohort of human clinical cases, we show that this mouse model system reproduces key histologic, immunohistochemical and molecular features of HPV-associated carcinosarcoma. While further studies are required to define the precise mechanisms underlying tumor development, this model provides a useful experimental platform for studying the pathogenesis and therapeutic vulnerabilities of HPV-associated carcinosarcoma.</p>","PeriodicalId":49095,"journal":{"name":"Cell and Bioscience","volume":" ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}