Journal of Cell Communication and Signaling最新文献_第4页

Favorable and poor prognosis B-cell precursor acute lymphoblastic leukemia subtypes reveal distinct leukemic cell properties when interacting with mesenchymal stem cells, differentially modifying their cell stemness and leukemia chemoresistance 预后良好和预后不良的b细胞前体急性淋巴细胞白血病亚型在与间充质干细胞相互作用时显示出不同的白血病细胞特性，不同地改变其细胞干性和白血病化疗耐药

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-12 DOI: 10.1002/ccs3.70009

Ángel Cortés Santiago, Rojas Zambrano Paula-Manuela, Vernot Jean-Paul

{"title":"Favorable and poor prognosis B-cell precursor acute lymphoblastic leukemia subtypes reveal distinct leukemic cell properties when interacting with mesenchymal stem cells, differentially modifying their cell stemness and leukemia chemoresistance","authors":"Ángel Cortés Santiago, Rojas Zambrano Paula-Manuela, Vernot Jean-Paul","doi":"10.1002/ccs3.70009","DOIUrl":"https://doi.org/10.1002/ccs3.70009","url":null,"abstract":"The development of B-ALL alters the bone marrow microenvironment influencing disease progression and response to therapy. The aggressiveness of particular B-ALL subtypes could be related to specific mechanisms used to reprogram bone marrow stromal cells. The purpose of this study is to compare the effect of two B-ALL subtypes, with opposite prognosis, on mesenchymal stem cells (MSC) functions and the consequences on leukemic cell properties. We have established an in vitro leukemic niche (LN) by co-culturing MSC with REH (favorable prognosis) or SUP-B15 (poor prognosis) B-ALL cell lines and examined leukemic-induced MSC reprogramming and its impact on leukemic cells properties and drug resistance. The aggressive SUP-B15 cell line showed faster and stronger adherence to MSC and increased migration to CXCL12 and LN secretome, compared to REH cells. SUP-B15 cell proliferation was reduced but modulated over time. No differences in MSC senescence induction or recovery were observed between both cell lines. Interestingly, the SUP-B15 LN secretome was enriched in IL-6, IL-8, CCL2 and MIF. MSC pre-incubated with CCL2 showed increased MSC senescence but this did not alter protection against cytotoxic drugs. On the contrary, MSC self-renewal and adipogenic differentiation were also increased in the aggressive SUP-B15 cell line, strengthening protection against the cytotoxic drugs vincristine, methotrexate and doxorubicin. This study showed that the aggressiveness of certain leukemia subtypes is also associated with specific changes induced in MSC secretome and stemness that have an impact on specific properties of leukemic cells, improving LN fitness and ability to survive to cytotoxic drugs.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Adipose-derived stem cell exosomes alleviate TGF-β1-induced urethral stricture fibrosis by suppressing the TGF-β/Smad pathway and downstream PDGFR-β/RAS/ERK signaling 脂肪源性干细胞外泌体通过抑制TGF-β/Smad通路和下游PDGFR-β/RAS/ERK信号通路减轻TGF-β1诱导的尿道狭窄纤维化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-12 DOI: 10.1002/ccs3.70025

Tao Liang, Chao Deng, Hang Guo, Zhenghao Dai, Yiwen Jiang, Yuting Lu, Weiguo Chen

{"title":"Adipose-derived stem cell exosomes alleviate TGF-β1-induced urethral stricture fibrosis by suppressing the TGF-β/Smad pathway and downstream PDGFR-β/RAS/ERK signaling","authors":"Tao Liang, Chao Deng, Hang Guo, Zhenghao Dai, Yiwen Jiang, Yuting Lu, Weiguo Chen","doi":"10.1002/ccs3.70025","DOIUrl":"https://doi.org/10.1002/ccs3.70025","url":null,"abstract":"This study aimed to investigate the therapeutic effects and underlying mechanisms of adipose-derived stem cell exosomes (ADSCs-exo) in ameliorating fibrosis in a rat model. ADSCs were isolated and cultured from rat adipose tissue, and ADSCs-exo were extracted via ultracentrifugation. Urethral fibrosis was induced by local injection of TGF-β1 (10 μg), followed by ADSCs-exo treatment. Urodynamic parameters were evaluated, and histological changes were evaluated using hematoxylin and eosin and Masson staining. Transcriptomic analysis and pathway enrichment were performed to identify signaling pathways regulated by ADSCs-exo. In vitro, urinary fibroblasts were stimulated with TGF-β1 and treated with ADSCs-exo alone or in combination with PDGF-BB (agonist) or imatinib (inhibitor). ADSCs-exo treatment significantly improved urodynamic function, reduced collagen deposition, and suppressed fibrosis-related protein expression in vivo. Transcriptomic analysis revealed platelet-derived growth factor and TGF-β pathways as major contributors to fibrosis. In vitro, ADSCs-exo significantly reduced TGF-β1-induced fibroblast proliferation, migration, and fibrosis-related protein expression, effects that were reversed by PDGF-BB and enhanced by imatinib. These findings were consistent in vivo, further supporting the hierarchical regulation of fibrosis-related signaling by ADSCs-exo. ADSCs-exo mitigates urethral stricture fibrosis by primarily suppressing the TGF-β/Smad pathway, thereby downregulating the downstream PDGFR-β/RAS/ERK axis, highlighting its therapeutic potential as a cell-free therapeutic approach for fibrotic urethral disease.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gut microbiota-derived trimethylamine-N-oxide inhibits SIRT1 to regulate SM22α-mediated smooth muscle cell inflammation and promote atherosclerosis progression 肠道微生物源性三甲胺- n -氧化物抑制SIRT1调节sm22 α介导的平滑肌细胞炎症，促进动脉粥样硬化进展

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-06 DOI: 10.1002/ccs3.70021

Yajuan Yin, Mei Wei, Xiufang Jiang, Mei Liu, Xiaocui Shi, Xiao Zhang, Le Wang, Gang Liu, Mingqi Zheng, Fangfang Ma

{"title":"Gut microbiota-derived trimethylamine-N-oxide inhibits SIRT1 to regulate SM22α-mediated smooth muscle cell inflammation and promote atherosclerosis progression","authors":"Yajuan Yin, Mei Wei, Xiufang Jiang, Mei Liu, Xiaocui Shi, Xiao Zhang, Le Wang, Gang Liu, Mingqi Zheng, Fangfang Ma","doi":"10.1002/ccs3.70021","DOIUrl":"https://doi.org/10.1002/ccs3.70021","url":null,"abstract":"Atherosclerosis (AS) is a prevalent cardiovascular disease, and emerging evidence highlights the critical role of gut microbiota in its development. Trimethylamine-N-oxide (TMAO), a metabolite derived from gut microbiota, is thought to promote AS progression by regulating smooth muscle protein 22-alpha (SM22α)-mediated inflammation in vascular smooth muscle cells. This study aims to explore the molecular mechanisms of TMAO in AS through multi-omics analysis, particularly its effects on SIRT1 inhibition and SM22α modulation. 16S ribosomal RNA sequencing revealed an altered gut microbiota composition in AS mice, characterized by increased Bacteroides and decreased Firmicutes. Metabolomics analysis indicated elevated levels of TMAO in AS mice. Transcriptomic data and cell experiments further confirmed that TMAO promotes AS by regulating SM22α-mediated inflammation via SIRT1 regulation. These findings suggest that TMAO accelerates progression through the SIRT1 and SM22α-related pathways, offering novel therapeutic targets for AS intervention.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endometriosis-derived exosomes encapsulated miR-196a-5p mediate macrophage polarization through regulation of the Hippo pathway 包裹miR-196a-5p的子宫内膜异位症衍生外泌体通过调节Hippo通路介导巨噬细胞极化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-05-25 DOI: 10.1002/ccs3.70020

Bin Lu, Qixiang Huang, Yanyu Zhong

{"title":"Endometriosis-derived exosomes encapsulated miR-196a-5p mediate macrophage polarization through regulation of the Hippo pathway","authors":"Bin Lu, Qixiang Huang, Yanyu Zhong","doi":"10.1002/ccs3.70020","DOIUrl":"https://doi.org/10.1002/ccs3.70020","url":null,"abstract":"Endometriosis (EMs) is a disease that adversely affects women's health. Immune imbalance is an important factor contributing to EMs, and exosomes (Exo) play an important role in immunomodulation. The purpose of this study was to investigate the effect of exosomes derived from the blood of patients with EMs on macrophage polarization and elucidate the underlying mechanisms. Exosomes were isolated from the serum of healthy controls (control exosomes) and patients with EMs (EMs exosomes). Macrophage polarization levels were detected using flow cytometry (FCM), RT-qPCR, and Western blot. Subsequently, we used RNA sequencing to analyze differential microRNAs (miRNA) and associated pathways. Electroporation techniques were used to modify the exosomes. The associated pathways were analyzed by Western blot. Finally, 12Z cells were co-cultured with macrophages of different polarizations, and the viability and metastasis of 12Z cells were calculated by cell counting kit-8 (CCK-8), scratch, and Transwell. EMs exosomes induced M2-type polarization in macrophages. RNA sequencing results showed that miR-196a-5p was dramatically decreased in EMs exosomes, whereas overexpression of miR-196a-5p in EMs exosomes could inhibit the M2-type polarization of macrophages and activate the Hippo pathway. In addition, M2-type macrophages promoted 12Z cell proliferation and metastasis. These findings suggest that serum-derived exosomes encapsulating miR-196a-5p alleviate endometriosis by promoting M1-type macrophage polarization via Hippo pathway activation.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ELAVL1 promotes ferroptosis via the TRIM21/HOXD8 axis to inhibit osteogenic differentiation in congenital pseudoarticular tibia-derived mesenchymal stem cells ELAVL1通过TRIM21/HOXD8轴促进铁凋亡，抑制先天性假关节胫骨源间充质干细胞的成骨分化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-05-21 DOI: 10.1002/ccs3.70016

Weihua Ye, Zheng Liu, Yaoxi Liu, Han Xiao, Qian Tan, An Yan, Guanghui Zhu

{"title":"ELAVL1 promotes ferroptosis via the TRIM21/HOXD8 axis to inhibit osteogenic differentiation in congenital pseudoarticular tibia-derived mesenchymal stem cells","authors":"Weihua Ye, Zheng Liu, Yaoxi Liu, Han Xiao, Qian Tan, An Yan, Guanghui Zhu","doi":"10.1002/ccs3.70016","DOIUrl":"https://doi.org/10.1002/ccs3.70016","url":null,"abstract":"Osteogenic differentiation of mesenchymal stem cells (MSCs) was strongly correlated with the progression of congenital tibial pseudoarthrosis (CPT). Activation of ferroptosis inhibited osteogenic differentiation of MSCs. ELAV-like RNA binding protein 1 (ELAVL1) is a key factor in promoting ferroptosis. This study aimed to elucidate the mechanism of ELAVL1 in the osteogenic differentiation of CPT periosteum-derived MSCs. Osteogenic differentiation of CPT periosteum-derived MSCs was detected by ARS and ALP staining. Fe2+ content and lipid reactive oxygen species content were measured using commercial kits. Molecular interactions were verified using RIP, RNA pulldown, and Co-IP. The ubiquitination level of homeobox gene D8 (HOXD8) was detected using Co-IP. Expression of ELAVL1 and tripartite motif containing 21 (TRIM21) was upregulated in CPT periosteum-derived MSCs, whereas HOXD8 expression was downregulated. Moreover, knockdown of ELAVL1 or TRIM21 inhibited ferroptosis and promoted osteogenic differentiation of CPT MSCs. TRIM21 overexpression reversed the effect caused by knockdown of ELAVL1. Mechanistically, ELAVL1 upregulated TRIM21 by increasing the stability of TRIM21, which ubiquitinated and degraded HOXD8. ELAVL1 bound to TRIM21, which promoted ubiquitination and degradation of HOXD8, thereby promoting ferroptosis to inhibit osteogenic differentiation of CPT MSCs.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144108765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Daphnetin alleviates inflammation and promotes autophagy via the AMPK/mTOR pathway in gouty arthritis 在痛风性关节炎中，瑞香素通过AMPK/mTOR通路减轻炎症并促进自噬

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-04-28 DOI: 10.1002/ccs3.70011

Zhiyong Liu, Aichun Chu, Zhiqian Bai, Chao Yang

{"title":"Daphnetin alleviates inflammation and promotes autophagy via the AMPK/mTOR pathway in gouty arthritis","authors":"Zhiyong Liu, Aichun Chu, Zhiqian Bai, Chao Yang","doi":"10.1002/ccs3.70011","DOIUrl":"https://doi.org/10.1002/ccs3.70011","url":null,"abstract":"Gouty arthritis (GA) is an inflammatory disease resulting from monosodium urate (MSU) crystal deposition in joints and surrounding tissues. Daphnetin (DAP) is a coumarin derivative with potent anti-inflammatory activity. Nonetheless, whether DAP can protect against MSU-induced acute GA remains unclarified. In this study, C57BL/6 mice were injected intra-articularly with MSU crystal suspension to induce acute GA. THP-1 cells were stimulated with MSU to mimic the microenvironment of GA in vitro. Hematoxylin–eosin staining was conducted to observe the pathological changes in mouse synovial tissues. ELISA and RT-qPCR were employed for inflammatory cytokine level determination. Immunofluorescence staining was performed to estimate LC3 expression in THP-1 cells. Western blotting was used for protein expression analysis. The results showed that DAP pretreatment mitigated MSU-elicited ankle joint swelling and synovial damage in mice. Moreover, DAP hindered proinflammatory factor expression and promoted autophagy in MSU-stimulated GA mice and THP-1 cells. Mechanistically, DAP induced AMPK activation and mTOR inactivation. Blocking AMPK signaling counteracted DAP-mediated effects on inflammation and autophagy in MSU-stimulated THP-1 cells. In conclusion, DAP prevents MSU-elicited GA by alleviating inflammation and enhancing autophagy via AMPK/mTOR signaling transduction.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143884128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CEP162: A critical regulator of ciliary transition zone assembly and its implications in ciliopathies CEP162：纤毛过渡区组装的关键调节因子及其在纤毛病中的意义

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-04-23 DOI: 10.1002/ccs3.70012

Jun Yin, Jialian Bai, Xiaochong He, Wenjuan He, Hongming Miao, Mengjie Zhang, Zhongying Yu, Bing Ni

{"title":"CEP162: A critical regulator of ciliary transition zone assembly and its implications in ciliopathies","authors":"Jun Yin, Jialian Bai, Xiaochong He, Wenjuan He, Hongming Miao, Mengjie Zhang, Zhongying Yu, Bing Ni","doi":"10.1002/ccs3.70012","DOIUrl":"https://doi.org/10.1002/ccs3.70012","url":null,"abstract":"CEP162, a 162-kDa centrosome protein, is a crucial centrosomal adapter, mediating cell differentiation and polarization. CEP162 maintains mitosis by dynamically stabilizing microtubules. CEP162 promotes the transition zone (TZ) assembly in the basal body through interaction with CEP131, CEP290, and axoneme microtubules as well as the distal centriole. TZ ensures the normal distribution of soluble proteins between the cytoplasm and cilia. It also facilitates retinal development and sperm flagellar motility. However, fluctuations in TZ permeability caused by abnormal expression of CEP162, including truncated mutations and naturally occurring mutations, lead to cilia abnormality and dysfunction in ciliogenesis through the regulation of intraflagellar transport, resulting in retinal degeneration and infertility. LncRNAs can induce SNP events in the CEP162 transcript by altering alternative splicing. Naturally occurring mutations are closely linked to retinal ciliopathy and diabetic retinopathy. This review summarizes the latest research progress to better understand the biology and pathophysiology of CEP162 and the clinical manifestations caused by CEP162 variants.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Macrophages-derived small extracellular vesicles regulate chondrocyte proliferation and affect osteoarthritis progression via upregulating Osteopontin expression 巨噬细胞衍生的细胞外小泡通过上调骨桥蛋白表达调节软骨细胞增殖并影响骨关节炎的进展

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-04-22 DOI: 10.1002/ccs3.70008

Min Tu, An-Min Liu, Wei Huang, Dan Wang, Hou-Qiong Chen, Xiao-Yuan Hu

{"title":"Macrophages-derived small extracellular vesicles regulate chondrocyte proliferation and affect osteoarthritis progression via upregulating Osteopontin expression","authors":"Min Tu, An-Min Liu, Wei Huang, Dan Wang, Hou-Qiong Chen, Xiao-Yuan Hu","doi":"10.1002/ccs3.70008","DOIUrl":"https://doi.org/10.1002/ccs3.70008","url":null,"abstract":"Small extracellular vesicles (sEVs) are considered promising gene-delivery vehicles for the treatment of osteoarthritis (OA). This study aimed to explore the molecular mechanism by which M2 macrophage-derived sEVs (M2-sEVs) modulate chondrocyte proliferation and apoptosis, thereby affecting OA progression. M2 macrophages were successfully induced, and M2-sEVs were successfully isolated. The sEVs were small vesicles with diameters ranging from 50 to 150 nm. The exosomal markers, including CD9, CD63, and CD81, were highly expressed, whereas the negative marker calnexin was absent in M2-sEVs. M2-sEVs effectively alleviated OA tissue and chondrocyte damage in both in vivo and in vitro models, evidenced by reduced rat knee joint injury, increased chondrocyte viability, and decreased chondrocyte apoptosis and extracellular matrix (ECM) degradation. Furthermore, M2-sEVs decreased the levels of pro-inflammatory cytokines IL-6 and TNF-α. Osteopontin (OPN) was upregulated within rats with OA and IL-1β-induced chondrocytes. Silencing of OPN exacerbated IL-1β-induced chondrocyte damage and partially abrogated the therapeutic effects of M2-sEVs. Additionally, M2-sEVs enhanced OPN expression and activated CD44 and the PI3K/AKT signaling pathway. In conclusion, M2-sEVs promoted OPN expression to improve knee joint tissue damage in rats with OA and chondrocyte damage. This protective effect of M2-sEVs might be associated with the activation of CD44 and the PI3K/AKT signaling.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Extracellular vesicle-LncRNA HOTAIR modulates esophageal cancer chemoresistance and immune microenvironment via miR-375/CDH2 pathway 细胞外囊泡- lncrna HOTAIR通过miR-375/CDH2途径调控食管癌化疗耐药和免疫微环境

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-04-14 DOI: 10.1002/ccs3.70014

Tayier Tuersong, Munire Shataer, Yan Chen, Gaosi Chen, Xiaoling Li, Linjie Lei, Ayiguli Younusi, Liangying Ma

{"title":"Extracellular vesicle-LncRNA HOTAIR modulates esophageal cancer chemoresistance and immune microenvironment via miR-375/CDH2 pathway","authors":"Tayier Tuersong, Munire Shataer, Yan Chen, Gaosi Chen, Xiaoling Li, Linjie Lei, Ayiguli Younusi, Liangying Ma","doi":"10.1002/ccs3.70014","DOIUrl":"https://doi.org/10.1002/ccs3.70014","url":null,"abstract":"Chemoresistance and immune evasion remain significant barriers to effective esophageal cancer (EC) treatment. This study explores the mechanistic role of extracellular vesicles (EVs) delivering LncRNA HOTAIR in modulating these processes. Using transcriptomic profiling, LncRNA HOTAIR was identified as a critical factor in EC progression. Its interaction with miR-375 was examined via luciferase reporter assays and RNA immunoprecipitation. Paclitaxel-resistant EC cells were treated with EVs containing HOTAIR, and the functional impact on proliferation, migration, invasion, and immune response was assessed through in vitro and in vivo models. LncRNA HOTAIR in EVs enhanced paclitaxel resistance by suppressing miR-375 and increasing CDH2 expression. Furthermore, HOTAIR promoted immune escape by upregulating PD-L1, impairing T-cell-mediated cytotoxicity. These changes were validated in patient-derived EC models. This study demonstrates that EV-LncRNA HOTAIR mediates chemoresistance and immune evasion in EC by targeting the miR-375/CDH2 axis. These findings provide a foundation for novel therapeutic interventions targeting EV-HOTAIR.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143831068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NS3 of hepatitis C virus drives hepatocellular carcinoma progression through a novel RNA-interference pathway 丙型肝炎病毒NS3通过一种新的rna干扰途径驱动肝细胞癌进展

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-04-12 DOI: 10.1002/ccs3.70013

Yajun Liang, Jian Luo, Liya Hu, Jun Zhang

{"title":"NS3 of hepatitis C virus drives hepatocellular carcinoma progression through a novel RNA-interference pathway","authors":"Yajun Liang, Jian Luo, Liya Hu, Jun Zhang","doi":"10.1002/ccs3.70013","DOIUrl":"https://doi.org/10.1002/ccs3.70013","url":null,"abstract":"Hepatocellular carcinoma (HCC), a severe consequence of hepatitis C virus infection, is significantly influenced by the virus’s non-structural protein 3 (NS3). This study employed transcriptome sequencing to explore the role of NS3 in promoting HCC progression by comparing gene expression profiles between HCV-infected HCC tissues and healthy liver controls. Key genes regulated by NS3 were identified and validated with quantitative reverse transcription PCR (RT-qPCR) and western blot analyses. Functionality assays, including CCK-8, BrdU, and Transwell migration and invasion tests, were performed to evaluate the effects of NS3 on HCC cell proliferation, migration, and invasion. Further investigation through a dual-luciferase reporter and RNA pull-down assays revealed that NS3 specifically upregulates circ_0001175. This circular RNA interacts with and inhibits miR-130a-5p, diminishing its regulatory impact on P53 by modulating the MDM4 pathway, thereby promoting oncogenic characteristics. The findings highlight the NS3-induced circ_0001175/miR-130a-5p/MDM4/P53 pathway as a potential therapeutic target, offering promising directions for treatment strategies in HCV-related HCC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143824726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0