Experimental cell research最新文献_第10页

Hsa_circ_0081111 promotes the proliferation and metastasis of non-small cell lung cancer by regulating IGF2BP2-mediated stability of Slug mRNA Hsa_circ_0081111通过调节igf2bp2介导的Slug mRNA的稳定性，促进非小细胞肺癌的增殖和转移。

IF 3.5 3区生物学

Experimental cell research Pub Date : 2025-07-15 DOI: 10.1016/j.yexcr.2025.114685

Wenjun Tang , Junnv Xu , Shu Lin, Jingru Luo, Xiaohong Zhuang, Xiaoying Qian, Chengsheng Zhang

{"title":"Hsa_circ_0081111 promotes the proliferation and metastasis of non-small cell lung cancer by regulating IGF2BP2-mediated stability of Slug mRNA","authors":"Wenjun Tang , Junnv Xu , Shu Lin, Jingru Luo, Xiaohong Zhuang, Xiaoying Qian, Chengsheng Zhang","doi":"10.1016/j.yexcr.2025.114685","DOIUrl":"10.1016/j.yexcr.2025.114685","url":null,"abstract":"<div><div>Previous researches have indicated the oncogenic effect of circCOL1A2 in several cancers, such as tongue squamous cell carcinoma, gastric cancer, and colorectal cancer. Regrettably, the functions and mechanisms of circCOL1A2 in lung cancer, a disease with the highest global incidence and mortality rates and with 85 % of cases classified as non-small cell lung cancer (NSCLC), remain largely unexplored. Hsa_circ_0081111 (circCOL1A2) was identified from GSE236879 dataset of Gene Expression Omnibus (GEO) database. Its expression was validated in 37 paired samples of cancerous and adjacent normal tissues from NSCLC patients, as well as in cell lines. The function of hsa_circ_0081111 was analyzed using CCK-8, Matrigel transwell, Western blot, and immunofluorescence assays <em>in vitro</em>, and by conducting subcutaneous xenograft experiments in mouse. The underlying mechanisms were explored using bioinformatics analysis, RNA pull-down experiments, and RNA immunoprecipitation. High expression of hsa_circ_0081111 was observed in NSCLC tissues and cell lines. This was positively correlated with the TNM stage and lymph node metastasis of NSCLC patients. Hsa_circ_0081111 overexpression promoted the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of NSCLC cells. Conversely, its downregulation showed the opposite effects. <em>In vivo</em> studies revealed that silencing hsa_circ_0081111 inhibited tumor growth, EMT, and MMP9 expression in tumor tissues. Mechanically, hsa_circ_0081111 enhanced Slug mRNA stability by interacting with the RNA-binding protein IGF2BP2. Taken together, hsa_circ_0081111 is an oncogenic circRNA that promotes NSCLC malignancy by regulating IGF2BP2-mediated Slug mRNA stability. Hsa_circ_0081111 has the potential to be a diagnostic and therapeutic target for NSCLC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114685"},"PeriodicalIF":3.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

“TFEB–HNRNPA2B1”: A positive feedback loop facilitating metastasis in hepatocellular carcinoma cells “TFEB-HNRNPA2B1”：一个促进肝癌细胞转移的正反馈回路

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-07-08 DOI: 10.1016/j.yexcr.2025.114669

Xiaojing Yan , Yaran Wu , Xufang Dai , Huizhong Wen , Wei Xiang , Mingzhen Yang , Yang Zhang , Li Xiang , Lu Lu , An Chen , Fengtian He , Jiqin Lian

{"title":"“TFEB–HNRNPA2B1”: A positive feedback loop facilitating metastasis in hepatocellular carcinoma cells","authors":"Xiaojing Yan , Yaran Wu , Xufang Dai , Huizhong Wen , Wei Xiang , Mingzhen Yang , Yang Zhang , Li Xiang , Lu Lu , An Chen , Fengtian He , Jiqin Lian","doi":"10.1016/j.yexcr.2025.114669","DOIUrl":"10.1016/j.yexcr.2025.114669","url":null,"abstract":"<div><div>This study elucidated the regulatory role of the TFEB-HNRNPA2B1 feedback loop in hepatocellular carcinoma (HCC) metastasis, a highly prevalent and aggressive liver cancer subtype. The findings demonstrated that transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, was significantly upregulated in HCC tissues, particularly in advanced-stage tumors and lymph node metastatic lesions. Functional studies revealed that TFEB overexpression enhanced metastatic potential in HCC cell lines, whereas its genetic knockdown substantially suppressed metastatic capacity. Mechanistic investigations identified HNRNPA2B1 as a critical mRNA stabilizer of TFEB, establishing a reciprocally reinforcing feedback loop wherein TFEB transactivated HNRNPA2B1 expression. This autoregulatory circuit drove metastatic progression through coordinated upregulation of pro-metastatic genes, ultimately promoting HCC cell dissemination. These results suggested therapeutic targeting of the TFEB-HNRNPA2B1 axis as a promising strategy for inhibiting liver cancer metastasis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114669"},"PeriodicalIF":3.3,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144588166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The phosphorylation of moesin impairs the integrity of vascular basement membrane in pathological angiogenesis 在病理性血管生成中，moesin的磷酸化损害了血管基底膜的完整性

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-07-07 DOI: 10.1016/j.yexcr.2025.114668

Jiaqing Hu , Zhuanhua Liu , Xiaoxia Huang , Bingyu Li , Zhenfeng Chen , Tairan Zeng , Xing Zhou , Qiaobing Huang

{"title":"The phosphorylation of moesin impairs the integrity of vascular basement membrane in pathological angiogenesis","authors":"Jiaqing Hu , Zhuanhua Liu , Xiaoxia Huang , Bingyu Li , Zhenfeng Chen , Tairan Zeng , Xing Zhou , Qiaobing Huang","doi":"10.1016/j.yexcr.2025.114668","DOIUrl":"10.1016/j.yexcr.2025.114668","url":null,"abstract":"<div><div>Our previous studies demonstrated that advanced glycation end products (AGEs) promote angiogenesis in human umbilical vein endothelial cells (HUVECs) and mouse retina through moesin phosphorylation. AGEs-induced angiogenesis is characterized by abnormal VE-cadherin distribution at adherens junctions and decreased pericytes coverage. In this study, we further investigated the alterations in collagen IV (Col-IV) distribution within the basement membrane (BM) of neovesssles using a HUVECs-retinal microvascular pericytes (RMPs) co-culture system and an AGEs-treated mouse model. The role of moesin phosphorylation in AGEs-induced BM abnormalities was explored through phosphorylation modulation. The results confirmed that AGEs-induced immature angiogenesis in HUVECs-RMPs co-culture system, characterized by decreased pericyte coverage and uneven Col-IV distribution in the neovessel BM. Similar results were observed in retinal vessels from AGEs-treated mice. Modulation of moesin phosphorylation altered the AGEs-induced maldistribution of Col-IV in the vascular BM. We observed obvious co-localization of phosphorylated moesin with heterogenous adhesion molecule CD44 in mouse retinal vessels. This study demonstrates that AGEs induce abnormal distribution of Col-IV in the vascular BM and subsequent neovessel immaturity via phosphorylation of moesin and disruption of heterogenous adhesion junction formation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114668"},"PeriodicalIF":3.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144579301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

K542 acetylation promotes YTHDF2 binding to m6A-modified mRNAs and fosters colorectal cancer progression K542乙酰化促进YTHDF2与m6a修饰的mrna结合并促进结直肠癌的进展

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-07-05 DOI: 10.1016/j.yexcr.2025.114667

Bo Wen , Shiwei Feng , Lin Bao , Sheng Li , Yanping Yang , Shiyou Long , Jian Xiao , Shujuan Li , Yujie Hou , Sisi Liu

{"title":"K542 acetylation promotes YTHDF2 binding to m6A-modified mRNAs and fosters colorectal cancer progression","authors":"Bo Wen , Shiwei Feng , Lin Bao , Sheng Li , Yanping Yang , Shiyou Long , Jian Xiao , Shujuan Li , Yujie Hou , Sisi Liu","doi":"10.1016/j.yexcr.2025.114667","DOIUrl":"10.1016/j.yexcr.2025.114667","url":null,"abstract":"<div><div>N6-methyladenosine (m6A) modification serves as a crucial regulator of diverse biological processes and disease progression. A central player in m6A regulation is YT521-B homology domain family member 2 (YTHDF2), a well-characterized m6A-binding protein primarily involved in mRNA stabilization. This study identifies lysine 542 (K542) as a critical acetylation site on YTHDF2, regulated by p300 as the acetyltransferase and SIRT2 as the deacetylase. Notably, while K542 acetylation has minimal effects on YTHDF2's protein stability or subcellular localization, it significantly enhances the protein's binding affinity for m6A-modified mRNAs. This enhanced binding affinity has profound biological implications, as K542 acetylation promotes malignant phenotypes in colorectal cancer (CRC) cells in vitro and <em>in vivo</em>. Supporting its clinical relevance, analysis of CRC tissues reveals elevated levels of YTHDF2 acetylation in primary tumors, strongly associating this modification with CRC pathology. Collectively, these findings highlight K542 acetylation as a key enhancer of YTHDF2's m6A recognition and a critical driver of its oncogenic activity.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114667"},"PeriodicalIF":3.3,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144579245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Comparative analysis of 3D culture methodologies in prostate cancer cells 前列腺癌细胞三维培养方法的比较分析。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-07-01 DOI: 10.1016/j.yexcr.2025.114666

Ella Foster , Oliver Wardhana , Ziyu Zeng , Xin Lu

{"title":"Comparative analysis of 3D culture methodologies in prostate cancer cells","authors":"Ella Foster , Oliver Wardhana , Ziyu Zeng , Xin Lu","doi":"10.1016/j.yexcr.2025.114666","DOIUrl":"10.1016/j.yexcr.2025.114666","url":null,"abstract":"<div><div>Three-dimensional (3D) cell culture models are increasingly utilized in cancer research to better replicate in vivo tumor microenvironments. This study examines the effects of different 3D scaffolding materials, including Matrigel, GelTrex, and the plant-based GrowDex, on prostate cancer cell lines, with a particular emphasis on neuroendocrine prostate cancer (NEPC). Four cell lines (LNCaP, LASCPC-01, PC-3, and KUCaP13) were cultured in these scaffolds using the sandwich method to evaluate spheroid formation, cell viability, and gene expression. The results revealed that while all scaffolds supported cell viability, spheroid formation varied significantly: Matrigel promoted the most consistent spheroid formation, exhibiting the best results for LASCPC-01 among the tested scaffolds, though spheroid formation for LASCPC-01 was generally more limited than for LNCaP. Gene expression analysis indicated a reduction in androgen receptor (<em>AR</em>) expression in LNCaP cells across all scaffolds using the sandwich method. However, further experiments using a mini-dome method revealed that the expression of AR signaling genes and neuroendocrine marker genes varied depending on the scaffolds and culture methods. These findings highlight the scaffold-dependent variability in 3D culture outcomes and emphasize the need for standardized methodologies to ensure consistency and relevance in prostate cancer research.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114666"},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Timosaponin AIII alleviates type 2 diabetes-induced cardiomyopathy by targeting galectin-3 (LGALS3) Timosaponin AIII通过靶向半凝集素-3 （LGALS3）缓解2型糖尿病诱导的心肌病

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-06-30 DOI: 10.1016/j.yexcr.2025.114665

Jing Yin , Chenxi Yu , Zhongyong Zhang , Jialin Cong

{"title":"Timosaponin AIII alleviates type 2 diabetes-induced cardiomyopathy by targeting galectin-3 (LGALS3)","authors":"Jing Yin , Chenxi Yu , Zhongyong Zhang , Jialin Cong","doi":"10.1016/j.yexcr.2025.114665","DOIUrl":"10.1016/j.yexcr.2025.114665","url":null,"abstract":"<div><div>Timosaponin AIII, the main active saponin derived from <em>Anemarrhena asphodeloides</em> Bunge, exerts anti-diabetic effects. However, its underlying mechanism in diabetic cardiomyopathy (DCM) remains unclear. In this study, we explored the pharmacological effects of timosaponin AIII on DCM using a mouse model and H9c2 cells. We found that timosaponin AIII treatment attenuated cardiac remodeling, myocardial fibrosis, and cardiomyocyte apoptosis in high-fat diet (HFD) combined with streptozotocin (STZ)-induced diabetic mice. Additionally, it significantly reduced galectin-3 expression in HFD/STZ-induced heart tissue and HG-exposed H9c2 cells. Mechanistically, timosaponin AIII facilitated the ubiquitin-dependent degradation of galectin-3. Notably, in timosaponin AIII-treated H9c2 cells, overexpression of galectin-3 significantly restored cardiomyocyte apoptosis and oxidative stress. Taken together, our data confirmed that timosaponin AIII demonstrated cardioprotective effects in diabetic mice by reducing fibrosis and apoptosis. These findings suggest a promising pharmacological strategy for treating DCM.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114665"},"PeriodicalIF":3.3,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144536162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

FMR1 KH0-KH1 domains coordinate m6A binding and phase separation in Fragile X syndrome FMR1 KH0-KH1结构域在脆性X综合征中协调m6A结合和相分离

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-06-28 DOI: 10.1016/j.yexcr.2025.114664

Xian Zhou , Chen-Jun Guo , Rui Wang , Yi-Lan Li , Tianyi Zhang , Zhuangyi Qiu , Shaorong Gao , Ji-Long Liu , Yawei Gao

引用次数: 0

Cathepsin S mediates the disruption of airway epithelial Pannexin 1 via an Akt-dependent pathway in an LPS-induced murine model of acute lung injury 在lps诱导的小鼠急性肺损伤模型中，组织蛋白酶S通过akt依赖途径介导气道上皮Pannexin 1的破坏

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-06-28 DOI: 10.1016/j.yexcr.2025.114663

Changyun Yang , Lin Fu , Rui Li , Haixiong Tang , Zemin Chen , Sudan Gan , Jiamin Sun , Shiyue Li , Jing Li , Lihong Yao

{"title":"Cathepsin S mediates the disruption of airway epithelial Pannexin 1 via an Akt-dependent pathway in an LPS-induced murine model of acute lung injury","authors":"Changyun Yang , Lin Fu , Rui Li , Haixiong Tang , Zemin Chen , Sudan Gan , Jiamin Sun , Shiyue Li , Jing Li , Lihong Yao","doi":"10.1016/j.yexcr.2025.114663","DOIUrl":"10.1016/j.yexcr.2025.114663","url":null,"abstract":"<div><div>Airway epithelial dysfunction constitutes a pivotal contributor to the pathogenesis of acute lung injury (ALI). Pannexin 1 (Panx1), a plasma membrane channel activated during epithelial injury, not only helps dampen inflammation but also plays a key role in epithelial repair. Cathepsin S (CTSS) is implicated in ALI pathophysiology. This study investigates the mechanistic link between CTSS and airway epithelial Panx1 dysregulation in ALI pathogenesis. Lipopolysaccharide (LPS) was instilled into the airways of BALB/c mice, followed by intraperitoneal injection of the CTSS inhibitor LY3000328. The effects of recombinant mouse CTSS (rCTSS) were tested in vivo, and Akt inhibition was used to explore the possible mechanism. In vitro, LPS-treated BEAS-2B cells were co-cultured with or without CTSS or Akt inhibitors. LPS exposure significantly increased pulmonary expression of CTSS. Treatment with LY3000328 alleviated the LPS-induced neutrophil accumulation, alveolar permeability and edema. Additionally, we observed decreased expression of Panx1 in the airway epithelium of LPS-exposed mice, accompanied by increased serine phosphorylation of Akt (p-Akt); inhibition of CTSS restored Panx1 and suppressed the p-Akt. Treatment with rCTSS directly downregulated Panx1 expression and induced Akt phosphorylation in the lung, which could be reversed by pharmacological inhibitor of Akt. In BEAS-2B cells, LPS increased CTSS and p-Akt expression alongside decreased levels of junction proteins (E-cadherin and occludin) and Panx1. Blockade of the CTSS/Akt axis restored the disruption of E-cadherin, occludin, and Panx1. Taken together, our data demonstrated that CTSS regulates the dysregulation of airway epithelial Panx1 through the Akt signaling pathway in an LPS-induced ALI model.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114663"},"PeriodicalIF":3.3,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144518341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Immunomodulatory, anti-synoviocyte, and anti-osteoclastic abilities of embryonic stem cell-derived mesenchymal stem cells in rheumatoid arthritis 类风湿关节炎中胚胎干细胞衍生间充质干细胞的免疫调节、抗滑膜细胞和抗破骨能力。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-06-27 DOI: 10.1016/j.yexcr.2025.114660

Eun-Yeong Bok , Won-Jae Lee , HyeonJeong Lee , Chan-Hee Jo , Chae-Yeon Hong , Seo-yoon Kang , Sanghyeon Park , Tae-Sung Hwang , Jaemin Kim , Sung-Lim Lee , Yong-Ho Choe , Sang-Il Lee

{"title":"Immunomodulatory, anti-synoviocyte, and anti-osteoclastic abilities of embryonic stem cell-derived mesenchymal stem cells in rheumatoid arthritis","authors":"Eun-Yeong Bok , Won-Jae Lee , HyeonJeong Lee , Chan-Hee Jo , Chae-Yeon Hong , Seo-yoon Kang , Sanghyeon Park , Tae-Sung Hwang , Jaemin Kim , Sung-Lim Lee , Yong-Ho Choe , Sang-Il Lee","doi":"10.1016/j.yexcr.2025.114660","DOIUrl":"10.1016/j.yexcr.2025.114660","url":null,"abstract":"<div><div>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation, fibroblast-like synoviocyte hyperactivation, and osteoclast-mediated bone destruction. Mesenchymal stem cells (MSCs) derived from adult tissues exhibit therapeutic potential owing to their regenerative and immunomodulatory properties; However, commercialization remains challenging due to limitations in large-scale production with consistent quality. Contrastingly, MSCs derived from embryonic stem cells can be continuously produced and exhibit minimal variation, with high biological and genetic uniformity. We confirmed that DW-MSCs exhibit MSC characteristics, including proliferative capacity, surface marker expression, and immunomodulatory function in vitro, by comparison with umbilical cord-derived MSCs (UC-MSCs) as one representative type of adult tissue-derived MSCs. We further evaluated their effects on RA pathology via in vitro assays of FLS migration and osteoclastogenesis. Although DW-MSCs showed lower immunosuppressive capacity than UC-MSCs, DW-MSCs retained functional immunosuppressive efficacy and exhibited superior inhibition of FLS migration and osteoclastogenesis, both of which are critical in the complex pathogenesis of RA. In a collagen-induced arthritis mouse model, intra-articular injection of DW-MSCs reduced inflammation and bone erosion, with an increased regulatory T cell/T-helper-17 ratio in draining lymph nodes. These findings demonstrated the therapeutic potential of DW-MSCs and support their application as a scalable and standardized stem cell-based treatment for RA.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114660"},"PeriodicalIF":3.3,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The NF-κB/LY6E axis promotes oral squamous cell carcinoma stemness by responding to interaction with macrophages NF-κB/LY6E轴通过与巨噬细胞相互作用促进口腔鳞状细胞癌的发生。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-06-27 DOI: 10.1016/j.yexcr.2025.114661

Yan Hu , Yongle Qiu , Wenjing Wang , Xin He , Qian Wu , Tianyi Cai , Shuojing Lu , Zhizheng Zhuang

{"title":"The NF-κB/LY6E axis promotes oral squamous cell carcinoma stemness by responding to interaction with macrophages","authors":"Yan Hu , Yongle Qiu , Wenjing Wang , Xin He , Qian Wu , Tianyi Cai , Shuojing Lu , Zhizheng Zhuang","doi":"10.1016/j.yexcr.2025.114661","DOIUrl":"10.1016/j.yexcr.2025.114661","url":null,"abstract":"<div><div>Cancer stemness plays a pivotal role in driving metastasis and recurrence in oral squamous cell carcinoma (OSCC). Although immune-tumor cell interactions regulate cancer stemness plasticity, the underlying mechanisms remain incompletely characterized. This study aimed to explore the key signaling axis mediating tumor-immune cell crosstalk that governs cancer stemness in OSCC. Single-cell RNA sequencing (scRNA-seq) data from the Gene Expression Omnibus (GEO) database revealed eight major cell clusters and five epithelial sub-clusters within OSCC. CytoTRACE analysis revealed that epithelial sub-cluster 1 exhibiting the highest stemness potential, from which ten stemness-related genes were derived. Among these, <em>LY6E</em> was screened as an enhancer-controlled gene in OSCC cells. LY6E knockdown significantly suppressed self-renewal and proliferation of OSCC cells <em>in vitro</em>, as well as tumor growth <em>in vivo</em>. Mechanistically, NF-κB bound to the enhancer of <em>LY6E</em> to drive its transcription. Cell-cell communication analysis highlighted that macrophages are the dominant immune cells interacting with malignant cells. Macrophage-derived TNFα facilitated NF-κB enrichment at the <em>LY6E</em> enhancer regions and upregulated its transcription in OSCC cells. TNFα stimulation, exposure to macrophage-conditioned medium, or coculture with macrophages significantly promoted the self-renewal and proliferation of OSCC cells, but these effects were abolished by LY6E knockdown or NF-κB inhibition. In conclusion, the NF-κB/LY6E axis is a key signaling hub in response to macrophage-OSCC cell interaction in promoting cancer stemness.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"450 2","pages":"Article 114661"},"PeriodicalIF":3.3,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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