Cellular signalling最新文献_第10页

LncRNA AFAP1-AS1 promoting residual tumor progression after insufficient radiofrequency ablation by up-regulating macropinocytosis in hepatocellular carcinoma LncRNA AFAP1-AS1通过上调肝细胞癌巨噬细胞增多症促进射频消融不足后残留肿瘤进展。

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-29 DOI: 10.1016/j.cellsig.2025.112031

Qiuxia Wei , Shiyu Xiong , Wanrong Luo , Qi Zhang , Sui Zheng , Man Luo , Haifeng Tang , Wenyue Zhang , Baoming Luo

{"title":"LncRNA AFAP1-AS1 promoting residual tumor progression after insufficient radiofrequency ablation by up-regulating macropinocytosis in hepatocellular carcinoma","authors":"Qiuxia Wei , Shiyu Xiong , Wanrong Luo , Qi Zhang , Sui Zheng , Man Luo , Haifeng Tang , Wenyue Zhang , Baoming Luo","doi":"10.1016/j.cellsig.2025.112031","DOIUrl":"10.1016/j.cellsig.2025.112031","url":null,"abstract":"<div><h3>Background</h3><div>The impact of macropinocytosis on residual tumor progression following insufficient radiofrequency ablation (IRFA) in hepatocellular carcinoma (HCC) remains uncertain.</div></div><div><h3>Objectives</h3><div>It is very important to further investigate the regulatory mechanism of macropinocytosis after IRFA in HCC.</div></div><div><h3>Methods</h3><div>We established cellular and animal models of IRFA using heat-treated HCC cells and subcutaneous tumors. In addition, we evaluated macropinocytosis level via FITC-dextran uptake, analyzed RNA expression by RT-qPCR, assessed proteins expression through Western blot, and performed functional assays. We also explored 5-(N-ethyl-N-isopropyl)-amiloride (EIPA, a pharmacological blocker of macropinocytosis) and LncRNA AFAP1-AS1 effects on tumor growth in animal models.</div></div><div><h3>Results</h3><div>We demonstrated that IRFA increased macropinocytosis in both HCC cells and xenografted HCC tissues. EIPA markedly suppressed the proliferation, migration, and invasion of HCC cells and suppressed residual tumor growth. Furthermore, We found that AFAP1-AS1 expression was significantly elevated following IRFA in the tissues of HCC patients and HCC cell lines due to the increase in m6A modification. An increase in AFAP1-AS1 expression correlated with heightened macropinocytosis activity. Mechanistically, AFAP1-AS1 indirectly increased EGFR expression by interacting with and reducing the levels of miR-139-5p, thereby contributing to residual tumor progression post-IRFA through the upregulation of macropinocytosis.</div></div><div><h3>Conclusions</h3><div>Our findings revealed AFAP1-AS1's oncogenic role and proposed its potential as a diagnostic marker and therapeutic candidate for residual tumor progression and macropinocytosis suppression in HCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112031"},"PeriodicalIF":3.7,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759295","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}

引用次数: 0

G protein-coupled estrogen receptor promotes human extravillous trophoblast invasion via YAP-Snail-mediated CYR61 expression G蛋白偶联雌激素受体通过yap -蜗牛介导的CYR61表达促进人胞外滋养细胞侵袭

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-29 DOI: 10.1016/j.cellsig.2025.112033

Hailong Wang , Xiaoyu Han , Ze Wu, Manman Guo, Siwei Luo, Lanlan Fang, Jung-Chien Cheng

{"title":"G protein-coupled estrogen receptor promotes human extravillous trophoblast invasion via YAP-Snail-mediated CYR61 expression","authors":"Hailong Wang , Xiaoyu Han , Ze Wu, Manman Guo, Siwei Luo, Lanlan Fang, Jung-Chien Cheng","doi":"10.1016/j.cellsig.2025.112033","DOIUrl":"10.1016/j.cellsig.2025.112033","url":null,"abstract":"<div><div>Preeclampsia (PE) is a pregnancy-related disorder characterized by impaired extravillous trophoblast (EVT) invasion, leading to defective placental development. The G protein-coupled estrogen receptor (GPER) is expressed in human EVT cells and has been implicated in promoting cell invasion. Cysteine-rich angiogenic inducer 61 (CYR61), also known as CCN1, is a matricellular protein that facilitates cell migration and invasion; however, whether GPER activation regulates CYR61 expression in EVT cells remains undefined. In this study, we investigated the molecular mechanisms underlying GPER-mediated regulation of CYR61 in human EVT cells. We demonstrated that activation of GPER by its selective agonist G1 upregulated CYR61 expression in both HTR-8/SVneo and primary human EVT cells. Mechanistically, GPER activation enhanced YAP signaling, leading to the upregulation of Snail, which was required for CYR61 expression. Functional assays revealed that CYR61 was essential for EVT cell invasion, as its knockdown significantly reduced G1-stimulated cell invasion. Furthermore, analysis of publicly available single-cell RNA sequencing (scRNA-seq) data showed that CYR61 expression was significantly downregulated in EVT cells from PE placentas. Our findings identify a novel GPER-YAP-Snail-CYR61 signaling axis that regulates EVT invasion and suggest that dysregulation of this pathway may contribute to defective trophoblast invasion in PE.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112033"},"PeriodicalIF":3.7,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144749852","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}

引用次数: 0

Enhanced 5-methylcytosine methylation of PSD4 facilitates vasculogenic mimicry in breast cancer brain metastases through ferroptotic resistance PSD4的5-甲基胞嘧啶甲基化增强通过铁致耐药促进乳腺癌脑转移的血管生成模拟

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-28 DOI: 10.1016/j.cellsig.2025.112022

Min Li , Chuanyou Cui , Jiawei Li , Jianfeng Zhou , Shen Chen , Jinqiang Yan , Di Zhang , Yifei Zhang , Panpan Xie , Yumin Yao , Feixue Ni , Meng An , Wei Zhang , Bo Fu

{"title":"Enhanced 5-methylcytosine methylation of PSD4 facilitates vasculogenic mimicry in breast cancer brain metastases through ferroptotic resistance","authors":"Min Li , Chuanyou Cui , Jiawei Li , Jianfeng Zhou , Shen Chen , Jinqiang Yan , Di Zhang , Yifei Zhang , Panpan Xie , Yumin Yao , Feixue Ni , Meng An , Wei Zhang , Bo Fu","doi":"10.1016/j.cellsig.2025.112022","DOIUrl":"10.1016/j.cellsig.2025.112022","url":null,"abstract":"<div><div>During the metastatic progression of cancer, tumor cells undergo widespread genetic and epigenetic alterations. The regulatory mechanism of 5-methylcytosine (m<sup>5</sup>C) methylation of PSD4 in breast cancer brain metastasis (BCBM) remains unclear. In this study, we found that PSD4 expression is markedly elevated in both BCBM tissues and cell lines. Functional assays <em>in vitro</em> revealed that overexpression of PSD4 significantly promoted cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition (EMT). Complementary <em>in vivo</em> experiments confirmed the tumor-promoting and metastasis-enhancing roles of PSD4 in brain metastases. At the mechanistic level, PSD4 m<sup>5</sup>C methylation was regulated by NSUN2 <em>via</em> its catalytic domains (C271A/C321A), which enhanced PSD4 mRNA stability and facilitated its nuclear export, increasing its expression. Furthermore, YBX1 was identified as a critical m<sup>5</sup>C-binding protein regulating PSD4 methylation. Functional analysis also showed that PSD4 contributes to vasculogenic mimicry (VM) by promoting ferroptosis resistance, decreasing vascular permeability, and enhancing tumor growth and metastasis to the brain. These findings establish PSD4 as a key player in BCBM and suggest its potential as a diagnostic marker and therapeutic target.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112022"},"PeriodicalIF":3.7,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738884","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}

引用次数: 0

Bavachinin alleviates allergic rhinitis by modulating gut microbiota and inhibiting NLRP3-mediated epithelial pyroptosis through PI3K/AKT/NF-κB signaling pathway 巴伐利亚蛋白通过PI3K/AKT/NF-κB信号通路调节肠道菌群，抑制nlrp3介导的上皮细胞焦亡，从而缓解变应性鼻炎

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-28 DOI: 10.1016/j.cellsig.2025.112026

Tian Chen , Lin Dong , Yang Wu , Tao Shen , Yuqin Deng , Fen Li , Zezhang Tao

{"title":"Bavachinin alleviates allergic rhinitis by modulating gut microbiota and inhibiting NLRP3-mediated epithelial pyroptosis through PI3K/AKT/NF-κB signaling pathway","authors":"Tian Chen , Lin Dong , Yang Wu , Tao Shen , Yuqin Deng , Fen Li , Zezhang Tao","doi":"10.1016/j.cellsig.2025.112026","DOIUrl":"10.1016/j.cellsig.2025.112026","url":null,"abstract":"<div><div>Allergic rhinitis (AR), a chronic, non-infectious nasal mucosal inflammation, for which there is no drug that can completely cure it. Bavachinin (BVC), a natural bioactive flavanone from Psoraleae Fructus, has anti-inflammatory and anti-asthmatic properties. However, its effects on AR and the associated mechanism remain unclear. In this study, network pharmacology and molecular docking results showed that AR treatment outcomes using BVC are closely related to the PI3K– Akt pathway and that BVC has a strong binding affinity for NLRP3 and PI3K. BVC showed significant therapeutic effects on AR-model mice, manifesting significant relief of nasal disease signs, suppression of the allergic inflammatory response, a reduction in nasal epithelial pyroptosis, and restoration of the epithelial barrier function. Furthermore, after BVC treatment, the disrupted gut microbiota of AR-model mice showed a tendency to recover, and the intestinal barrier-related protein expression was upregulated. In vitro experiments showed that BVC effectively inhibited the LPS-induced expression of proinflammatory factors. In addition, BVC counteracted the downregulated expression of ZO-1 and Claudin-1. The protective effect of BVC was found to be primarily derived from its inhibitory effect on the PI3K/AKT/NF-κB pathway, thereby suppressing classical NLRP3 inflammasome-mediated pyroptosis. In conclusion, these results indicate that BVC alleviates AR primarily by suppressing NLRP3-mediated pyroptosis via the PI3K/AKT/NF-κB pathway to restore nasal epithelial barrier functions and concomitant restoration of the gut microbiota composition.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112026"},"PeriodicalIF":3.7,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144738949","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}

引用次数: 0

Gambogic acid induces ferroptosis and suppresses colorectal cancer progression by modulating the m6A modification of p62 藤黄酸通过调节m6A修饰p62诱导铁下垂并抑制结直肠癌的进展。

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-26 DOI: 10.1016/j.cellsig.2025.112024

Jinshuang Wang , Jun Deng , Baihan Sun , Guanglei Qiao , Jing Yang , Zhen Gao , Qi Zhang , Min Dong , Pengfei Qu , Zhenxin Wang

{"title":"Gambogic acid induces ferroptosis and suppresses colorectal cancer progression by modulating the m6A modification of p62","authors":"Jinshuang Wang , Jun Deng , Baihan Sun , Guanglei Qiao , Jing Yang , Zhen Gao , Qi Zhang , Min Dong , Pengfei Qu , Zhenxin Wang","doi":"10.1016/j.cellsig.2025.112024","DOIUrl":"10.1016/j.cellsig.2025.112024","url":null,"abstract":"<div><div>Ferroptosis has emerged as a novel therapeutic target in cancer treatment. RNA N6-methyladenosine (m6A) methylation, plays a critical role in regulating ferroptosis and mediating tumor progression and therapy resistance. Gambogic acid (GA), a plant-derived compound with potent antitumor activity, was investigated for its role in inducing ferroptosis in colorectal cancer (CRC). In this study, we demonstrated that GA induces ferroptosis in CRC cells, as evidenced by increased Fe<sup>2+</sup>, reactive ROS, and MDA levels, alongside reduced GSH levels. These effects were reversed by ferroptosis inhibitors, iron chelators and autophagy inhibitors. Mechanistically, GA reduced global m6A contents by downregulating methyltransferase3 (METTL3) expression. Overexpression of METTL3 reversed GA-induced ferroptosis and associated biochemical changes. Importantly, METTL3-mediated m6A modification enhanced the stability of p62 mRNA in an IGF2BP1-dependent manner. GA decreased METTL3 protein stability through the ubiquitin-proteasomal degradation. Collectively, these findings reveal that GA induces ferroptosis in CRC by modulating METTL3-mediated m6A modification of p62, connecting RNA epigenetics to autophagy-ferroptosis crosstalk. This study provides novel insights into the therapeutic potential of targeting the METTL3/p62 axis for ferroptosis-based cancer therapy.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112024"},"PeriodicalIF":3.7,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144728342","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}

引用次数: 0

A STAT1-GBP3-STING positive feedback loop governs inflammation, oxidative stress, and DNA damage to trigger acute aortic dissection STAT1-GBP3-STING正反馈回路控制炎症、氧化应激和DNA损伤，从而引发急性主动脉夹层

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-24 DOI: 10.1016/j.cellsig.2025.112015

Si-ming Bu , Wen-li Wang , Yi-mei Liu , Qing Li , Jing-yu Sun , Xu-rao Zhao , Xu-bin Miao , Yong-bo Zhao , Ya-pei Zhao , Zhi-xue Song , Dong Ma

{"title":"A STAT1-GBP3-STING positive feedback loop governs inflammation, oxidative stress, and DNA damage to trigger acute aortic dissection","authors":"Si-ming Bu , Wen-li Wang , Yi-mei Liu , Qing Li , Jing-yu Sun , Xu-rao Zhao , Xu-bin Miao , Yong-bo Zhao , Ya-pei Zhao , Zhi-xue Song , Dong Ma","doi":"10.1016/j.cellsig.2025.112015","DOIUrl":"10.1016/j.cellsig.2025.112015","url":null,"abstract":"<div><div>Acute aortic dissection (AAD) is a degenerative aortic remodeling disease characterized by exceedingly high mortality without effective pharmacologic therapies. Although oxidative stress, DNA damage, and inflammation are associated with AAD, the precise interplay among these responses has remained unclear. In this study, aortas from mouse AD models were subjected to integrative ATAC-seq and RNA-seq analysis. The pathogenic targets governing oxidative stress, DNA damage, and inflammation were identified by single-cell RNA sequencing, ROS staining, chromatin immunoprecipitation combined with PCR (ChIP-PCR), and co-immunoprecipitation (CoIP) analysis in the IFN-γ-stimulated vascular smooth muscle cells (VSMCs), mouse AAD model, and human ascending aortas. The transcriptional profiles of 191 differentially expressed genes revealed the IFN-γ response, oxidative stress-related NOD-like receptor, STING signaling pathways and marked elevation of STAT1, activated inflammation, DNA damage and ROS. Mechanistically, the activation of STAT1 binding on promoters of GBP3, H2aX and IFN-γ gene in nuclear as well as the interaction of GBP3 and STING protein in cytoplasm, determining a STAT1-GBP3-STING positive feedback loop triggering inflammation, DNA damage, and oxidative stress. Targeting this loop using STAT1 inhibitor Fludarabine impedes aortic degeneration while improving survival (60 % vs. 90 %) and reducing aortic expansion (2.34 ± 0.18 mm vs. 1.55 ± 0.15 mm) in the mouse AAD model. This study provides novel insights into a transcriptional program permitting aortic degeneration, warranting consideration of a critical target STAT1 for an anti-inflammation, anti-DNA damage, and anti-oxidative stress intervention as an attractive strategy to manage temporal-specific AD by modulating the STAT1-GBP3-STING positive feedback loop.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112015"},"PeriodicalIF":4.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144712495","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}

引用次数: 0

The biological clock gene PER2 promotes PANoptosis in oral squamous cell carcinoma by facilitating the formation of the Caspase-8/RIPK3/ASC complex 生物钟基因PER2通过促进Caspase-8/RIPK3/ASC复合物的形成，促进口腔鳞状细胞癌的PANoptosis

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-24 DOI: 10.1016/j.cellsig.2025.112021

Hengyan Li, Mingyuan Liu, Shilin Yin, Zhiwei Zhang, Kai Yang

{"title":"The biological clock gene PER2 promotes PANoptosis in oral squamous cell carcinoma by facilitating the formation of the Caspase-8/RIPK3/ASC complex","authors":"Hengyan Li, Mingyuan Liu, Shilin Yin, Zhiwei Zhang, Kai Yang","doi":"10.1016/j.cellsig.2025.112021","DOIUrl":"10.1016/j.cellsig.2025.112021","url":null,"abstract":"<div><div>Current research indicates that the circadian clock gene PER<em>2</em> plays a significant role in preventing tumor. However, its specific mechanism of action in oral squamous cell carcinoma (OSCC) remains unclear. While it is known that PANoptosis is critical for tumor suppression, whether PER2 exerts its anti-cancer effects by regulating this process has not been determined. Through bioinformatics analysis, our analysis revealed that PANoptosis-related genes (<em>MAP3K7</em>, <em>CASP8</em>) significantly correlate with the prognosis of OSCC patients. In OSCC cell lines (NOK, CAL27, SCC25, SCC15) and clinical samples, <em>PER2</em> expression demonstrated an extremely positive correlation with <em>CASP8</em> and a negative association with <em>MAP3K7</em>. The overexpression of PER2 significantly suppressed OSCC cell proliferation, promoted apoptosis, and increased both lactate dehydrogenase release and the expression of PANoptosis markers (cleaved caspase-3, N-GSDME, p-MLKL). In agreement with the in vitro findings, tumor xenograft experiments in vivo demonstrated that elevated PER2 expression inhibits tumor growth and upregulates the expression of PANoptosis markers. Mechanistically, PER2 binds to and stabilizes Caspase-8 protein, facilitating formation of the Caspase-8/RIPK3/ASC complex in OSCC cells. Notably, treatment with the Caspase-8 inhibitor <em>Z</em>-IETD-FMK markedly reversed PANoptosis in OSCC cells. This study provides the first evidence that PER2 overexpression suppresses OSCC proliferation by regulating the Caspase-8/RIPK3/ASC complex-mediated PANoptosis, offering a promising therapeutic strategy for OSCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112021"},"PeriodicalIF":4.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144713990","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}

引用次数: 0

Role of 3-mercaptopyruvate sulfurtransferase in cancer 3-巯基丙酮酸硫转移酶在癌症中的作用。

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-24 DOI: 10.1016/j.cellsig.2025.112020

Xue-Li Wang , Lei Cao , Yan-Wen Wang , Ti Chu , Yong-Qi Fan , Yu-Hang Chen , Yi Zhang , Wei-Rong Si , Qi-Ying Jiang , Dong-Dong Wu

{"title":"Role of 3-mercaptopyruvate sulfurtransferase in cancer","authors":"Xue-Li Wang , Lei Cao , Yan-Wen Wang , Ti Chu , Yong-Qi Fan , Yu-Hang Chen , Yi Zhang , Wei-Rong Si , Qi-Ying Jiang , Dong-Dong Wu","doi":"10.1016/j.cellsig.2025.112020","DOIUrl":"10.1016/j.cellsig.2025.112020","url":null,"abstract":"<div><div>The enzyme 3-mercaptopyruvate sulfurtransferase (3-MST) is widely distributed across different biological entities and is essential for the production of hydrogen sulfide (H₂S). This enzyme functions both in the cytosol and mitochondria, and 3-MST mediates the reaction of 3-mercaptopyruvate (3-MP) with dihydrolipoic acid and thioredoxin to generate hydrogen sulfide. In addition to 3-MST, H₂S can also be produced through the actions of cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE). H₂S, a gaseous signaling molecule with therapeutic potential, has been found to have therapeutic and alleviating effects on various diseases, including cancer, cardiovascular diseases, and neurological disorders. While the roles of CBS and CSE in cancer have been extensively studied and well-characterized, relatively little information is available in the scientific literature regarding the function and significance of 3-MST in cancer. This article focuses on the role of 3-MST in breast cancer, lung cancer, bladder cancer, and colon cancer, highlighting its potential as a therapeutic target.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 112020"},"PeriodicalIF":3.7,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717578","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}

引用次数: 0

Crosstalk between hippo and Wnt pathways in intestinal stem cells regeneration 肠干细胞再生中hippo和Wnt通路的串扰。

IF 3.7 2区生物学

Cellular signalling Pub Date : 2025-07-24 DOI: 10.1016/j.cellsig.2025.112023

Yanqiu Li, Yujun Hou, Yue He, Kexin Cheng, Ying Chen, Ying Li, Siyuan Zhou

引用次数: 0

PDCD4 exacerbates myocardial ischemia-reperfusion injury via AKT-mediated apoptosis PDCD4通过akt介导的细胞凋亡加重心肌缺血再灌注损伤

IF 4.4 2区生物学

Cellular signalling Pub Date : 2025-07-23 DOI: 10.1016/j.cellsig.2025.111999

Zhiming Zhang , Zhihui Yang , Hangbin Ge , Chenyang Liu , Renchenghan Fan , Chenying Yuan , Shengban You , Chenglv Hong

{"title":"PDCD4 exacerbates myocardial ischemia-reperfusion injury via AKT-mediated apoptosis","authors":"Zhiming Zhang , Zhihui Yang , Hangbin Ge , Chenyang Liu , Renchenghan Fan , Chenying Yuan , Shengban You , Chenglv Hong","doi":"10.1016/j.cellsig.2025.111999","DOIUrl":"10.1016/j.cellsig.2025.111999","url":null,"abstract":"<div><div>Myocardial ischemia-reperfusion (I/R) injury is a critical complication following reperfusion therapy for myocardial infarction. As a marker of I/R injury, apoptosis plays an important role in myocardial ischemia-reperfusion injury. Programmed Cell Death 4 (PDCD4) regulates apoptosis in MI/RI, but the mechanism is not yet fully elucidated. In this study, we demonstrate that PDCD4 expression was significantly upregulated in a myocardial I/R injury model. Genetic deletion of PDCD4 markedly reduced infarct size, serum biomarkers of injury (CK-MB, cTnT, LDH), and apoptosis in vivo. Mechanistically, PDCD4 directly interacts with AKT, inhibiting its phosphorylation by reducing ubiquitination. This suppression of AKT activity decreased BCL-2 levels, promoting mitochondrial apoptosis. Silencing PDCD4 restored AKT phosphorylation, attenuated apoptosis, and alleviated myocardial damage. Our findings establish PDCD4 as a key driver of myocardial I/R injury via AKT-mediated apoptosis and highlight its therapeutic potential.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"135 ","pages":"Article 111999"},"PeriodicalIF":4.4,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144704779","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}

引用次数: 0