Cell Proliferation最新文献

{"title":"A Specific tRNA Half, 3'tiRNA-GlyGCC, Regulates Hypoxic Pulmonary Artery Smooth Muscle Cell Proliferation via Myrf-Mediated Endoplasmic Reticulum Stress","authors":"Lixin Zhang,&nbsp;Xiaoyu Guan,&nbsp;Xiangrui Zhu,&nbsp;Yingying Hao,&nbsp;Ya Xu,&nbsp;Hao Yuan,&nbsp;Danni Gao,&nbsp;Hongxia Du,&nbsp;Jiayu Li,&nbsp;Weiwei Cao,&nbsp;Cui Ma,&nbsp;Xiaoying Wang","doi":"10.1111/cpr.70238","DOIUrl":"10.1111/cpr.70238","url":null,"abstract":"<p>Pulmonary artery smooth muscle cell (PASMC) proliferation is a hallmark of the pathogenesis of hypoxic pulmonary hypertension (PH), and endoplasmic reticulum stress (ERS) plays a crucial role. Many studies have implicated that tRNA-derived fragment, tiRNAs, in a variety of biological processes, but their roles in hypoxia-induced PASMC ERS and proliferation have not been investigated. In this study, we identified a significantly upregulated 3′tiRNA-GlyGCC in hypoxic mouse lung tissues using Arraystar small RNA microarray analysis. Functional assays, including CCK8, EdU incorporation, Western blot, and immunofluorescence, demonstrated that inhibition of 3′tiRNA-GlyGCC reversed hypoxia-induced ERS and proliferation in PASMCs. Mechanistically, 3′tiRNA-GlyGCC interacts with the eukaryotic translation elongation factor 1 alpha 1 (Eef1a1) protein and reduces the binding capacity between Eef1a1 and myelin regulatory factor (Myrf) mRNA, leading to decreased stability of Myrf mRNA. Additionally, 3′tiRNA-GlyGCC targets Myrf mRNA and inhibits its expression. We further verified that angiogenin (Ang) mediated the biogenesis of 3′tiRNA-GlyGCC under hypoxic conditions. Collectively, these findings highlight a novel mechanism underlying PASMC ERS and proliferation and suggest that 3′tiRNA-GlyGCC could serve as a potential therapeutic target for hypoxic PH.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053037","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}

{"title":"Human Gallbladder Cancer Organoids","authors":"Dongxi Xiang,&nbsp;Ting Gong,&nbsp;Yinjie Zhu,&nbsp;Bin Jia,&nbsp;Chen Zhang,&nbsp;Ning Tang,&nbsp;Weiping Wang,&nbsp;Yalong Wang,&nbsp;Laiping Zhong,&nbsp;Yanmei Zou,&nbsp;Jian Zhang,&nbsp;Zunqiang Zhou,&nbsp;Ligang Xing,&nbsp;Changchun Zhou,&nbsp;Dongyuan Zhu,&nbsp;Zengjun Liu,&nbsp;Gang Chen,&nbsp;Xiaoguang Wang,&nbsp;Zhan Wang,&nbsp;Aina He,&nbsp;Yonggang Wang,&nbsp;Zebing Liu,&nbsp;Jiabei Wang,&nbsp;Feng Xu,&nbsp;Ganglong Gao,&nbsp;Xiaonan Kang,&nbsp;Shuai Gong,&nbsp;Xianming Kong,&nbsp;Chunyan Dong,&nbsp;Aijin Ma,&nbsp;Gengming Niu,&nbsp;Guiying Wei,&nbsp;Hongling Zhao,&nbsp;Xiongxiong Lu,&nbsp;Jie Cao,&nbsp;Tongbiao Zhao,&nbsp;Zizhen Zhang,&nbsp;Yingbin Liu","doi":"10.1111/cpr.70211","DOIUrl":"10.1111/cpr.70211","url":null,"abstract":"<p>This guideline provides standardized requirements and quality control measures for human gallbladder cancer organoids, supporting their reliable application in research and precision medicine. It aims to promote methodological consistency, facilitate international collaboration, and accelerate translational research and clinical implementation.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13519846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825850","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}

{"title":"A Multicellular Coordinated Network Driving Lymphovascular Space Invasion in Endometrioid Endometrial Carcinoma","authors":"Wendi Guo,&nbsp;Tianxiang Liu,&nbsp;Runling Ren,&nbsp;Na Li,&nbsp;Wenwen Zhang,&nbsp;Jingwen Si,&nbsp;Yongjun Piao,&nbsp;Yuanjing Hu","doi":"10.1111/cpr.70246","DOIUrl":"10.1111/cpr.70246","url":null,"abstract":"<p>Lymphovascular space invasion (LVSI) is a critical factor linked to metastasis and poor outcomes in endometrioid endometrial carcinoma (EEC), yet its multicellular mechanisms remain unclear. Using single-cell RNA sequencing of 3 LVSI-present (LVSI+) EECs, 2 LVSI-absent (LVSI−) EECs, and 2 normal endometrial samples, we delineated the cellular ecosystems underlying LVSI. LVSI+ EECs exhibited marked epithelial reprogramming, transitioning from differentiated ciliated epithelium to hyperproliferative and metabolically remodelled phenotypes, and contained TC4, a metastatic epithelial subset characterized by hypoxia, partial epithelial–mesenchymal transition, immunosuppression, and progesterone resistance. We also identified nine key genes in malignant epithelial cells associated with LVSI prognosis. The tumour microenvironment in LVSI+ EECs shifted from an inflammatory state dominated by epithelial cells to a collaborative network involving stromal and immune cells. This network was enriched in immunosuppressive ZNF683 + SOX4 + CD8+ T cells, Cycling_T cells, SPP1 + MMP9 + Mac, WNT5A_mCAF, Tip endothelial cells, and lymphatic endothelial cells. WNT5A_mCAF and SPP1 + MMP9 + Mac synergistically remodelled the extracellular matrix, promoted lymphangiogenesis and angiogenesis, and, together with endothelial cells, suppressed T-cell activity via LGALS9–HAVCR2/CD44 inhibitory signalling, thereby establishing a niche conducive to vascular invasion. Using spatial multiplex immunofluorescence, we confirmed hypoxic tumour epithelial cells at the invasive front coexisting with an immunosuppressive microenvironment, and revealed spatial colocalization of PD-L1+ tumour cells, PD-L1+ macrophages, and PD-1+ T cells within LVSI thrombi. Our comprehensive study provides deeper insights into LVSI as an actively coordinated multicellular process, potentially improving LVSI risk prediction, supporting treatment decision-making, and informing new therapies targeting the tumour microenvironment.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307060","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}

{"title":"Periodontitis-Associated Circulating EVs Promote Colorectal Cancer Progression via Carnosine-Mediated Acidosis Adaptation","authors":"Ruoyi Wu,&nbsp;Zihan Cai,&nbsp;Hualing Sun,&nbsp;Haikun Yu,&nbsp;Bicheng Zhang,&nbsp;Chi Zhang,&nbsp;Yi Fan,&nbsp;Xiaoxuan Zhu,&nbsp;Yueqi Ni,&nbsp;Yu Cui,&nbsp;Kaixin Wang,&nbsp;Zhe Li,&nbsp;Xinyi Zhou,&nbsp;Qing He,&nbsp;Yanru Wu,&nbsp;Yufeng Zhang","doi":"10.1111/cpr.70254","DOIUrl":"10.1111/cpr.70254","url":null,"abstract":"<p>Colorectal cancer (CRC) is the third most common malignancy worldwide. Epidemiological studies have suggested a positive association between periodontitis (PD) and CRC risk; however, the mechanistic basis underlying this relationship remains unclear. Extracellular vesicles (EVs) represent an important mode of systemic communication and may mediate the distal effects between PD and CRC. PD model was established in <i>Apc</i>\u0000 ^{\u0000 <i>+/−</i>\u0000} mice with spontaneous intestinal tumorigenesis. Tumour onset, burden, and progression were evaluated in the colorectum and small intestine. Circulating EVs were isolated from the plasma of PD or sham mice and characterised. The functional contribution of EVs was assessed using pharmacological inhibition of EV release and MC38 syngeneic tumour models. Metabolomic profiling, RNA sequencing, and in vitro functional assays were performed to investigate EV cargo and underlying mechanisms. PD significantly accelerated CRC onset and increased tumour number and size in <i>Apc</i>\u0000 ^{\u0000 <i>+/−</i>\u0000} mice. Inhibition of EV release by GW4869 attenuated PD-driven tumour progression, indicating a critical role of periodontitis-associated EVs (PDEVs). PDEVs promoted tumour growth and induced an immunosuppressive tumour microenvironment in MC38 transplanted tumours. Metabolomic analysis revealed marked enrichment of carnosine in PDEVs. Under acidic conditions, EV-delivered carnosine alleviated intracellular acidosis, preserved lysosomal positioning and acidification, and promoted proliferation, migration, and epithelial–mesenchymal transition of MC38 cells. Collectively, circulating EV-mediated metabolic communication pathway linking PD to CRC progression. By delivering carnosine, PDEVs support malignant phenotypes and facilitate tumour adaptation to acidic stress. Circulating EV-associated carnosine may represent a potential biomarker and a candidate target for modulating CRC progression in high-risk populations.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366880","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}

{"title":"Featured Cover","authors":"Mengdie Xia,&nbsp;Man Li,&nbsp;Yanyu Chen,&nbsp;Jialin Chen,&nbsp;Yuting Cui,&nbsp;Xi-Long Zheng,&nbsp;Jing Yang,&nbsp;Bingzhao Li,&nbsp;Xiaofeng Ma,&nbsp;Miao Liu,&nbsp;Gang Fan,&nbsp;Juan Peng,&nbsp;Xiaoyan Dai,&nbsp;Zhihan Tang","doi":"10.1111/cpr.70298","DOIUrl":"https://doi.org/10.1111/cpr.70298","url":null,"abstract":"<p>The cover image is based on the article <i>Targeting PCSK9 in Vascular Smooth Muscle Cells: An Effective Strategy to Suppress Ferroptosis and Attenuate Abdominal Aortic Aneurysm Progression</i> by Mengdie Xia et al., https://doi.org/10.1111/cpr.70244.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cpr.70298","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149367532","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}

{"title":"Soluble Epoxide Hydrolase Inhibition Regulates Septoclast Activity to Promote Long Bone Growth and Fracture Healing by Enhancing Endothelial-to-Mesenchymal Notch Signalling","authors":"Weixian Chen,&nbsp;Liangliang Liu,&nbsp;Xumeng Wang,&nbsp;Juanjuan Li,&nbsp;Jingyi Zhang,&nbsp;Xiaoli Shi,&nbsp;Qing Sun,&nbsp;Xu Chang,&nbsp;Jing Zhang,&nbsp;Jie Zhao,&nbsp;Fu Wang","doi":"10.1111/cpr.70249","DOIUrl":"10.1111/cpr.70249","url":null,"abstract":"<p>Endochondral ossification is essential for the development of appendicular bones, physiological bone remodelling and fracture healing. Recent studies have identified mesenchymal stromal cell-derived FABP5⁺ septoclasts (SCs) as key mediators for the growth and repair of long bones, particularly in cartilage matrix degradation and growth plate remodelling via the secretion of matrix metalloproteinases. Our previous study has shown that soluble epoxide hydrolase (sEH) inhibitor, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), promotes long bone growth and bone repair by enhancing H-type vessel-coupled osteogenesis. However, whether TPPU treatment regulates SC activity, thereby promoting long-bone growth and fracture healing, remains unclear. Here, our in vitro and in vivo results showed that TPPU treatment promoted long-bone growth in newborn mice and regulated the hypertrophic layer in the growth plate, with a reduced ratio of hypertrophic cartilage (HC) to proliferative cartilage (PC) width. Furthermore, TPPU treatment enhanced SC activity, as evidenced by elevated expression of MMP9 and FABP5 in the metaphysis near the growth plate. Simultaneously, TPPU induced FABP5⁺ SC-like cells to degrade chondrocytes in co-cultured human umbilical vein endothelial cells (HUVECs) and human dental pulp stem cells (hDPSCs). Mechanistically, TPPU enhanced the crosstalk of co-cultured HUVECs and hDPSCs to activate the NOTCH signalling pathway in hDPSCs by upregulating HIF-1α expression in HUVECs. Furthermore, TPPU enhanced fracture healing by inducing more FABP5⁺ SCs and MMP9 secretion at the fracture site. Collectively, these findings highlight sEH as a promising therapeutic target that regulates endochondral ossification through inducing SC activity, offering new opportunities for bone development and repair.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257575","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}

{"title":"A 3D Bioprinted Platform That Maintains the Functional Integrity of Primary AML Cells","authors":"Wanling Huang,&nbsp;Bo Deng,&nbsp;Nini Guo,&nbsp;Yiyi Ding,&nbsp;Zhangjingwen Xu,&nbsp;Yiwen Lu,&nbsp;Yue Ma,&nbsp;Qian Ren,&nbsp;Nan Wang,&nbsp;Pengyu Huang,&nbsp;Xiaotong Ma","doi":"10.1111/cpr.70250","DOIUrl":"10.1111/cpr.70250","url":null,"abstract":"<p>Acute myeloid leukaemia (AML) urgently requires more reliable in vitro platforms for drug evaluation, as existing models often fail to maintain the phenotypic, metabolic, and pharmacologic features of primary leukaemic cells. To address this limitation, we developed a rapidly assembled, screening-compatible three-dimensional (3D) bioprinting platform. It encapsulates patient-derived bone marrow mononuclear cells within a gelatin-hyaluronic acid hydrogel, whose mechanical properties are tuned to match those of native bone marrow. Within this controlled 3D microenvironment, primary AML cells better maintain an in vivo-like state, showing enhanced viability, sustained proliferative capacity, preservation of stem-like subpopulations, and drug responses that more closely mirror clinical behaviour. Transcriptomic profiling further revealed robust activation of MYC target programs and mTORC1 signalling, accompanied by elevated oxidative phosphorylation and glycolytic activity, indicative of the highly proliferative and metabolically active state exhibited by AML cells in vivo. These findings demonstrate that our patient-specific, 3D bioprinted system provides a high-fidelity model. This model faithfully recapitulates AML physiology and metabolic features while capturing inter-patient variability. Consequently, it offers a more reliable and predictive platform for preclinical drug assessment.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13325942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263329","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}

{"title":"Optimising Haematopoietic Stem Cell Transplantation: Enhancing Myeloablation Sensitivity and Alleviating Anaemia Using Roxadustat (FG-4592)","authors":"Guanheng Yang,&nbsp;Jiahui Wu,&nbsp;Xinbing Guo,&nbsp;Wenchen Shen,&nbsp;Xiao Sang,&nbsp;Xiuli Gong,&nbsp;Shu-Zhen Huang,&nbsp;Jingzhi Zhang,&nbsp;Fanyi Zeng","doi":"10.1111/cpr.70230","DOIUrl":"10.1111/cpr.70230","url":null,"abstract":"<p>Haematopoietic stem cell transplantation (HSCT) is an effective therapy for a broad range of hematologic, autoimmune and genetic diseases. Successful HSCT requires adequate myeloablation to create space in the bone marrow microenvironment for donor haematopoietic stem and progenitor cells. Standard conditioning with busulfan and cyclophosphamide (BuCy), although widely used, may not completely clear recipient cells and can cause significant toxicity. Roxadustat (FG-4592), a hypoxia-inducible factor prolyl hydroxylase inhibitor used to treat renal anaemia, modulates HIF-1α stability and influences erythropoiesis, iron metabolism and cellular stress responses. Here, we investigated whether co-administration of FG-4592 during BuCy conditioning improves myeloablation efficiency and enhances donor-cell engraftment. Our results show that FG-4592 increases the sensitivity of bone marrow mononuclear cell (BM-MNC) populations to BuCy conditioning, promoting deeper depletion of both haematopoietic and non-haematopoietic recipient cells. This improved clearance supports enhanced donor-cell residency following transplantation. Furthermore, in <i>β</i>\u0000 ^{\u0000 <i>654</i>\u0000} thalassaemia mice, FG-4592 alleviated anaemia and reduced splenic iron deposition after HSCT. These findings suggest that FG-4592 can serve as an effective adjuvant to standard myeloablation regimens, supporting improved engraftment and hematologic recovery. To our knowledge, this is the first study demonstrating that a HIF-PH inhibitor can enhance conditioning efficiency during HSCT.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13352331/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419132","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}

{"title":"The E-cadherin-Wnt-mir-994 Axis Repurposes a Cadherin Switch for Niche Robustness and Germline Stem Cell Maintenance","authors":"Renjun Tu,&nbsp;Hiu Laam Yau,&nbsp;Runzhi Deng,&nbsp;Sarah E. Webb,&nbsp;Shiyuan Chen,&nbsp;Jianquan Ni,&nbsp;Ting Xie","doi":"10.1111/cpr.70245","DOIUrl":"10.1111/cpr.70245","url":null,"abstract":"<p>The resilience and robustness of the stem cell niche are critical for long-term tissue homeostasis, yet the molecular circuits that ensure this stability remain poorly understood. In the <i>Drosophila</i> ovarian germline stem cell niche, we investigate this fundamental question through the lens of adhesion, focusing on the role of N-cadherin in the somatic inner germarial sheath (IGS) cells. While the specific loss of N-cadherin alone is inconsequential, we discover that it becomes essential upon the loss of E-cadherin, revealing a critical, context-dependent function. This functional interplay is governed by a precise molecular circuit wherein E-cadherin cell-autonomously represses N-cadherin expression via a linear Wnt-<i>mir-994</i> signalling axis. Strikingly, this regulatory relationship constitutes a cadherin switch, which is repurposed within the niche not to promote dispersal, but to enforce resilience. The E-cadherin-to-N-cadherin switch acts as a vital compensatory mechanism: the ectopic upregulation of N-cadherin upon E-cadherin depletion is essential to maintain IGS cell survival and their long cellular processes, thereby rescuing niche integrity and preventing GSC loss. Our study defines the function for N-cadherin in IGS cells, unveils the E-cadherin-Wnt-<i>mir</i>-<i>994</i>-N-cadherin axis and demonstrates the repurposing of a classic developmental module as a robustness circuit to safeguard the stem cell niche. This repurposed cadherin switch reveals an axis for targeting the resilience of niche-stem cell interplay, and also informs new strategies for stabilizing niche environments in regenerative medicine or targeting the resilient cancer stem cell microenvironment.</p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148327345","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}

{"title":"Targeting CKIP-1 for Disease Therapy: Cellular Functions, Molecular Networks, and Clinical Potential","authors":"Xin Huang,&nbsp;Shijie Lv,&nbsp;Lejia Li,&nbsp;Jirong Xie,&nbsp;Zhengguo Cao","doi":"10.1111/cpr.70275","DOIUrl":"10.1111/cpr.70275","url":null,"abstract":"<p>CKIP-1, as a scaffold protein with special structural domains, treats related diseases through multiple emerging targeted technologies.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":9760,"journal":{"name":"Cell Proliferation","volume":"59 11","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860308","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}