Journal of Cell Communication and Signaling最新文献_第6页

IF 3.9 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-10

引用次数: 0

Homeobox B13 activates the hypoxia-inducible factor 1 pathway through histone lactylation thereby reprogramming lipid metabolism and promoting sorafenib resistance in hepatocellular carcinoma. Homeobox B13通过组蛋白乳酸化激活缺氧诱导因子1通路，从而重编程脂质代谢，促进肝细胞癌索拉非尼耐药。

IF 4 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-06 eCollection Date: 2026-06-01 DOI: 10.1002/ccs3.70077

Qingqing Xie, Fangxia Teng, Ting Ding, Huaizhe Zhang, Jian Huang, Shu Zhang

{"title":"Homeobox B13 activates the hypoxia-inducible factor 1 pathway through histone lactylation thereby reprogramming lipid metabolism and promoting sorafenib resistance in hepatocellular carcinoma.","authors":"Qingqing Xie, Fangxia Teng, Ting Ding, Huaizhe Zhang, Jian Huang, Shu Zhang","doi":"10.1002/ccs3.70077","DOIUrl":"10.1002/ccs3.70077","url":null,"abstract":"Resistance of hepatocellular carcinoma (HCC) to sorafenib represents a major clinical challenge, involving complex metabolic alterations and epigenetic regulatory changes. However, the underlying mechanisms remain incompletely understood. In this study, we found that the level of histone H3 lysine 18 lactylation (H3K18la), derived from lactate, was significantly elevated in sorafenib-resistant HCC cells. Mechanistically, using Micrococcal Nuclease-Chromatin Immunoprecipitation-quantitative Polymerase Chain Reaction and related techniques, we demonstrated that H3K18la is directly enriched at the promoter region of homeobox B13 (HOXB13) and functions as a potent transcriptional activator to upregulate its expression. Further mechanistic investigations revealed that HOXB13 stabilizes hypoxia-inducible factor-1α (HIF-1α) protein expression, thereby activating the HIF-1 signaling pathway, promoting lipid metabolism reprogramming, and enhancing lipid accumulation. Functional experiments demonstrated that the inhibition of H3K18la or knockdown of HOXB13 effectively reversed lipid accumulation and significantly increased cellular sensitivity to sorafenib. This study systematically delineates a signaling cascade (the H3K18la-HOXB13-HIF-1 axis) spanning metabolites, epigenetic modifications, transcriptional regulation, and downstream metabolic phenotypes, thereby deepening our understanding of tumor drug resistance mechanisms and providing potential therapeutic targets for overcoming HCC resistance to sorafenib.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 ","pages":"e70077"},"PeriodicalIF":4.0,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838528","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

IF 3.9 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-06

引用次数: 0

IF 3.9 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-03

引用次数: 0

Human brain pericytes protect the blood-brain barrier from triple-negative breast cancer cells while promoting tumor aggressiveness. 人脑周细胞保护血脑屏障免受三阴性乳腺癌细胞的侵袭，同时促进肿瘤的侵袭性。

IF 4 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-03 eCollection Date: 2026-06-01 DOI: 10.1002/ccs3.70070

Eloise Happernegg, Marine Carroué, Julien Cicero, Lucie Dehouck, Fumitaka Shimizu, Takashi Kanda, Chann Lagadec, Fabien Gosselet, Xuefen Le Bourhis, Maxime Culot, Robert-Alain Toillon, Caroline Mysiorek

{"title":"Human brain pericytes protect the blood-brain barrier from triple-negative breast cancer cells while promoting tumor aggressiveness.","authors":"Eloise Happernegg, Marine Carroué, Julien Cicero, Lucie Dehouck, Fumitaka Shimizu, Takashi Kanda, Chann Lagadec, Fabien Gosselet, Xuefen Le Bourhis, Maxime Culot, Robert-Alain Toillon, Caroline Mysiorek","doi":"10.1002/ccs3.70070","DOIUrl":"10.1002/ccs3.70070","url":null,"abstract":"The majority of breast cancer-related deaths result from metastatic progression, especially brain metastasis, associated with the poorest prognosis. Patients with triple-negative breast cancer (TNBC) are particularly prone to developing brain metastases. In this context, the blood-brain barrier (BBB) plays a pivotal role; however, the contribution of brain pericytes in mediating interactions between TNBC cells and the brain endothelial cells (ECs) remains unclear. To investigate the role of pericytes in modulating these interactions, we used a syngeneic human in vitro BBB model, composed of human brain-like endothelial cells (hBLECs) co-cultured with human brain pericytes (hBPs). Our findings demonstrate that hBPs secretions significantly reduce TNBC cell adhesion to hBLECs and protect the endothelium from TNBC cell-induced damage, both under normoxic and hypoxic conditions. Interestingly, we found that hBPs promote TNBC cell migration, invasion, and increase clonogenicity. Together, these findings uncover a dual role of brain pericytes in TNBC brain metastasis: they protect ECs and maintain BBB integrity against TNBC cells while simultaneously promoting tumor aggressiveness. Understanding this balance between protective and pro-metastatic functions may provide insights for developing novel therapeutic approaches to strengthen BBB defenses and limit brain colonization in TNBC patients.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":"e70070"},"PeriodicalIF":4.0,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838454","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

Integrative genomic and functional characterization of ADAMTS3 reveals its inflammatory regulation via NF-κB and STAT3 pathways in osteosarcoma. ADAMTS3的综合基因组和功能特征揭示了其在骨肉瘤中通过NF-κB和STAT3通路进行炎症调节。

IF 4 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-03 eCollection Date: 2026-06-01 DOI: 10.1002/ccs3.70072

Ehed Muhammed Aymaz, Meltem Alper, Feyza Nur Sav, Tuğşen Aydemir, Feray Köçkar

{"title":"Integrative genomic and functional characterization of ADAMTS3 reveals its inflammatory regulation via NF-κB and STAT3 pathways in osteosarcoma.","authors":"Ehed Muhammed Aymaz, Meltem Alper, Feyza Nur Sav, Tuğşen Aydemir, Feray Köçkar","doi":"10.1002/ccs3.70072","DOIUrl":"10.1002/ccs3.70072","url":null,"abstract":"Osteosarcoma (OS) is an aggressive bone malignancy characterized by genomic instability and extensive extracellular matrix (ECM) remodeling. Members of the ADAMTS family are matrix-associated proteases implicated in tumorigenesis; however, their roles in OS remain poorly defined. This study provides a comprehensive genomic, transcriptomic, and functional analysis of the ADAMTSs in OS, with particular focus on ADAMTS-3. Copy number alterations and mRNA expressions of ADAMTS genes were analyzed using the TCGA datasets. Gene set enrichment analysis and co-expression analyses identified biological processes associated with ADAMTS-3. Mechanistic studies investigated tumor necrosis factor-alpha (TNF-α) regulation of ADAMTS-3 in OS cells. Genomic profiling revealed frequent amplification and high mRNA expression of ADAMTS4, ADAMTS12, ADAMTS16, and ADAMTS17, indicating potential oncogenic activity. ADAMTS-3 was markedly overexpressed in OS tissues and cell lines, showing strong positive correlations with inflammatory (IL6, STAT3, NF-κB) and matrix-remodeling (MMP2, MMP9) genes. Functional enrichment indicated that ADAMTS-3 is associated with ECM organization, immune response regulation, and epithelial-mesenchymal transition. Mechanistically, TNF-α induced ADAMTS-3 transcription via activation of MEK, PI3K, JNK, and NF-κB pathways, with STAT3 and NF-κB by enhancing promoter activity. These findings identify ADAMTS-3 as an inflammation-responsive gene that links inflammatory signaling to ECM remodeling and tumor invasiveness in OS, representing a potential molecular bridge.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 2","pages":"e70072"},"PeriodicalIF":4.0,"publicationDate":"2026-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838505","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

IF 3.9 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-05-03

引用次数: 0

IF 3.9 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-04-30

引用次数: 0

P2X7 receptors promote atrial remodeling and atrial fibrillation susceptibility via reactive oxygen species-mediated mitogen-activated protein kinase signaling activation. P2X7受体通过活性氧介导的丝裂原活化蛋白激酶信号激活促进心房重构和心房颤动易感性。

IF 4 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-04-30 eCollection Date: 2026-06-01 DOI: 10.1002/ccs3.70071

Lingnan Zhang, Yeran Zhu, Xinshun Gu

{"title":"P2X7 receptors promote atrial remodeling and atrial fibrillation susceptibility via reactive oxygen species-mediated mitogen-activated protein kinase signaling activation.","authors":"Lingnan Zhang, Yeran Zhu, Xinshun Gu","doi":"10.1002/ccs3.70071","DOIUrl":"10.1002/ccs3.70071","url":null,"abstract":"Atrial fibrillation (AF), the most common clinical arrhythmia, is driven by inflammatory activation and oxidative stress, though precise molecular links remain unclear. This study identifies the P2X7 receptor as a key upstream regulator orchestrating proarrhythmic atrial remodeling through reactive oxygen species (ROS)-mediated mitogen-activated protein kinase (MAPK) signaling. Transcriptomic analysis of rapid-paced cardiomyocytes revealed P2X7 upregulation and MAPK pathway enrichment. Functional validation demonstrated that P2X7 activation promotes ROS accumulation, MAPK phosphorylation (p-ERK, p-p38, and p-JNK), and pro-inflammatory cytokine release (IL-6 and IL-1β), culminating in action potential shortening and calcium handling dysfunction. Critically, both P2X7 inhibition (A-438079) and ROS scavenging (NAC) attenuated this signaling axis. In vivo, P2X7 antagonism reduced AF susceptibility, improved conduction heterogeneity, and ameliorated structural and autonomic remodeling. These results establish the P2X7-ROS-MAPK axis as a central mechanism in AF vulnerability and highlight its therapeutic potential.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"20 ","pages":"e70071"},"PeriodicalIF":4.0,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815505","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

IF 3.9 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2026-04-25

引用次数: 0