Cellular signalling最新文献

{"title":"Y-box binding protein 1: A critical target for understanding and treating cardiovascular disease","authors":"Zixuan Liu ,&nbsp;Hongjie Wang ,&nbsp;Lei Dai ,&nbsp;Hesong Zeng ,&nbsp;Xiaodan Zhong","doi":"10.1016/j.cellsig.2025.111797","DOIUrl":"10.1016/j.cellsig.2025.111797","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) remain a significant public health burden, characterized by escalating morbidity and mortality rates and demanding novel therapeutic approaches. Cold shock protein Y-box binding protein 1 (YB-1), a highly conserved RNA/DNA-binding protein, has emerged as a pivotal regulator in various pathophysiological processes, including CVDs. YB-1 exerts pleiotropic functions by modulating gene transcription, pre-mRNA splicing, mRNA translation, and stability. The expression and function of YB-1 are intricately regulated by its subcellular localization, post-translational modifications, upstream regulatory signals. YB-1 plays a multifaceted role in CVDs, influencing inflammation, oxidative stress, cell proliferation, apoptosis, phenotypic switching of smooth muscle cells, and mitochondrial dysfunction. However, the regulation of YB-1 expression and function in CVDs is complex and context-dependent, exhibiting divergent effects even in the same disease across different cell types or at disease stages. This review comprehensively explores the structure, regulation, and functional significance of YB-1 in CVDs. We delve into the transcriptional and translational control mechanisms of YB-1, as well as its post-translational modifications. Furthermore, we elucidate the upstream signaling pathways that influence YB-1 expression, with a particular emphasis on non-coding RNAs and specific upstream molecules. Finally, we systematically examine the role of YB-1 in CVDs, summarizing its expression patterns, regulatory mechanisms, and therapeutic potential as a promising target for novel therapeutic interventions. By providing a comprehensive overview of YB-1's involvement in CVDs, this review aims to stimulate further research and facilitate the development of targeted therapies to improve cardiovascular health.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111797"},"PeriodicalIF":4.4,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143816353","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}

{"title":"Isoform specific regulation of osteopontin by AKT2 in hepatocytes and livers","authors":"Ielyzaveta Slarve ,&nbsp;Yushan Wang ,&nbsp;Yining Ding ,&nbsp;Xiaoteng Niu ,&nbsp;Qi Tang ,&nbsp;Chengyou Jia ,&nbsp;Taojian Tu ,&nbsp;Handan Hong ,&nbsp;Guo Zhang ,&nbsp;Yiwei Gu ,&nbsp;Zifei Xu ,&nbsp;Samantha Skinner ,&nbsp;Lina He ,&nbsp;Brittney Hua ,&nbsp;Phillip Nguyen ,&nbsp;Yiren Zhou ,&nbsp;Lulu Chen ,&nbsp;Karam Ashouri ,&nbsp;Anastasia Martynova ,&nbsp;Christina Nakhoul ,&nbsp;Bangyan Li Stiles","doi":"10.1016/j.cellsig.2025.111799","DOIUrl":"10.1016/j.cellsig.2025.111799","url":null,"abstract":"<div><div>Elevated levels of osteopontin (OPN), an inflammatory cytokine, are correlated with chronic inflammatory conditions and liver cancer. In this study, we explored the regulation of OPN in liver and hepatocytes by AKT1 vs. AKT2, the two AKT isoforms expressed in hepatocytes and livers. Using a mouse model lacking PTEN (phosphatase and tensin homologue deleted on chromosome 10), the negative regulator of phosphatidylinositol 3-kinase (PI3K)/AKT signaling, expression of secreted phosphoprotein 1 (<em>Spp1</em>), the gene encoding OPN, was found to be the topmost significantly upregulated gene in the liver. Using an add-back experiment in hepatocytes isolated from these mice, we show that PTEN regulates the expression of <em>Spp1</em> mRNA as well as OPN protein levels. Exploring how PTEN regulates the expression of <em>Spp1</em>/OPN, we investigated the differential roles of AKT1 vs. AKT2 using hepatocytes isolated from mice lacking each AKT isoform in the liver. We showed here that levels of <em>Spp1</em>/OPN in hepatocytes are lost with deletion of <em>Akt2</em> but not <em>Akt1</em>. Deletion of <em>Akt2</em> significantly attenuated both basal expression of OPN and its response to IGF-1 stimulation. AKT1 loss, on the other hand, permitted more robust induction of OPN by IGF-1 stimulation. Furthermore, mice lacking AKT2 and PTEN exhibit significantly lower OPN expression in the liver. Together, this study showed that OPN levels are regulated by the PI3K/AKT signal in hepatocytes and that AKT2 but not AKT1 is responsible for its induction in response to stimulation of the PI3K signaling pathway.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111799"},"PeriodicalIF":4.4,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143834245","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}

{"title":"Migrasomes: Critical players in intercellular nanovesicle communication","authors":"Jiayu Zhang ,&nbsp;Shoutao Weng ,&nbsp;Zaiwei Fan ,&nbsp;Dongyang Hu ,&nbsp;Jiadi Le ,&nbsp;Kongsheng Sheng","doi":"10.1016/j.cellsig.2025.111796","DOIUrl":"10.1016/j.cellsig.2025.111796","url":null,"abstract":"<div><div>Migrasomes are vesicular structures that form on elongated tethers originating from the tips or junctions of cellular tails during migration. These organelles, named for their vesicle rich lumen and release during cell movement, have gained attention for their role in intercellular communication and signal transduction. Migrasome formation is closely associated with the dynamic and active movement of cells, as well as with the intrinsic properties of cells and the extracellular microenvironment under various pathophysiological conditions. This review provides a comprehensive overview of migrasome dynamics, examining the mechanisms and distinct features of nanoscale vesicle-mediated intercellular signaling. It also highlights the influence of microscopic secretory factors on migrasome generation and formation. By comparing migrasomes with other active extracellular vesicles, this review highlights the advantages of migrasomes and addresses future challenges.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111796"},"PeriodicalIF":4.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807078","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}

{"title":"Regulation and function of inosine monophosphate dehydrogenase 2 cytoophidia during mouse and human decidualization","authors":"Yu-Ying He ,&nbsp;Dan-Dan Jin ,&nbsp;Bo Li ,&nbsp;Yue Li ,&nbsp;Meng-Yuan Li ,&nbsp;Gui-Jun Yan ,&nbsp;Zeng-Ming Yang","doi":"10.1016/j.cellsig.2025.111795","DOIUrl":"10.1016/j.cellsig.2025.111795","url":null,"abstract":"<div><div>Decidualization is essential for establishing pregnancy in both mice and humans. Cellular stresses, including nucleolar stress and DNA damage, are involved in this process. Inosine monophosphate dehydrogenase (IMPDH), the rate-limiting enzyme for de novo guanosine triphosphate (GTP) synthesis, forms membrane-free macromolecular structures called “cytoophidia” under specific conditions. However, whether IMPDH cytoophidia are present during decidualization remains unknown. In this study, we found that IMPDH2 cytoophidia are primarily detected in mouse decidual cells during early pregnancy. On day 5 of pregnancy, more IMPDH2 cytoophidia are observed at implantation sites than at inter-implantation sites. Physiologically, uteri activated by estrogen exhibit more IMPDH2 cytoophidia than those maintained in a delayed state by progesterone. Although GTP is required for in vitro decidualization in mice, elevated GTP level impairs this process. Furthermore, IMPDH2 cytoophidia can induce nucleolar stress and DNA damage in mice. In the human endometrium, IMPDH2 cytoophidia are observed during the menstrual cycle, particularly enriched in the secretory phase. They promote human decidualization and naturally enhance cellular senescence. Our findings highlight the physiological relevance of IMPDH2 cytoophidia during early pregnancy in mice and humans.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111795"},"PeriodicalIF":4.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829001","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}

{"title":"GRHL3 specifically initiated by the TP63 transcription factor promotes the metastasis of squamous cell carcinogenesis","authors":"Hanyu Bai ,&nbsp;Xiaojian Wei ,&nbsp;Xi Yan ,&nbsp;Sisi Wei ,&nbsp;Suli Dai ,&nbsp;Dachi Wang ,&nbsp;Yongxian Xue ,&nbsp;Debnarayan Jana ,&nbsp;Feng Gao ,&nbsp;Wei Zhou ,&nbsp;Lianmei Zhao","doi":"10.1016/j.cellsig.2025.111794","DOIUrl":"10.1016/j.cellsig.2025.111794","url":null,"abstract":"<div><div>Metastasis is the primary cause of death in squamous cell carcinoma (SCC) patients; thus, identification of highly sensitive tumor biomarkers and therapeutic targets that can be exploited to prevent SCC metastasis and clarification of the underlying molecular mechanism is critically important. Reports have shown that Grainyhead-like 3 (GRHL3) plays a crucial role in tumorigenesis and cancer progression; nevertheless, its functions and molecular mechanism in the development of cancer remain controversial. In the present study, GRHL3 was found to be specifically overexpressed in SCCs, including lung squamous cell carcinoma (LUSC), esophageal squamous cell carcinoma (ESCC), and cervical squamous cell carcinoma (CSCC). In particular, the study revealed that high GRHL3 expression is correlated with poor overall survival (OS) and progression-free survival (PFS) in LUSC patients. Functionally, GRHL3 knockdown suppressed the invasion and migration of SCC cells <em>in vitro</em> and decreased their lung metastasis potential <em>in vivo</em> but had little effect on cell proliferation. Mechanistically, the specific overexpression of GRHL3 in SCCs is orchestrated by a well-known oncogenic transcription factor: tumor protein p63 (TP63). GRHL3 stimulates the expression of heparanase (HPSE), thereby activating the AKT-SRC signaling axis. Taken together, our work reveals a novel molecular pathway through which GRHL3 mediates the metastasis of SCCs, which has important implications for the diagnosis and targeted treatment of SCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111794"},"PeriodicalIF":4.4,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807077","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}

{"title":"RIN1 regulates ferroptosis and nociceptive perception via the Nrf2/HO-1 pathway in chronic constriction injury","authors":"Xin Lin ,&nbsp;Xingyuan Li ,&nbsp;Shenglong Hong ,&nbsp;Qin Zhou ,&nbsp;Shan You","doi":"10.1016/j.cellsig.2025.111784","DOIUrl":"10.1016/j.cellsig.2025.111784","url":null,"abstract":"<div><div>Neuropathic pain (NP) has been a major focus of clinical research for decades. This study investigates the function of RAS- and RAB-interacting protein 1 (RIN1) in modulating NP and explore the involvement of the nuclear factor-2 erythroid factor-2 (Nrf2) and heme oxygenase 1 (HO-1) pathway in this context. A rat model of CCI was generated. The presence of mechanical and thermal hypersensitivity, as well as spontaneous pain behaviors, confirmed the successful modeling. Intrathecal injection of AAV9-shRNA targeting RIN1 attenuated nociception, reduced microglial activation in the L4-L6 spinal cord, and decreased the expression levels of c-Fos, GFAP, and IBA-1. Furthermore, the levels of NMDAR, PKC, Src, enzymes linked to neural hypersensitivity, was inhibited by RIN1 silencing. RIN1 was found to interact to Nrf2 protein, inhibiting its nuclear translocation and transcriptional activation. The RIN1 knockdown activated the Nrf2/HO-1 pathway, reducing oxidative stress and ROS levels in the spinal cord, while increasing the expression of Nrf2-target genes, including Nqo1, Gclc, and Gclm, which are key players in cellular antioxidant defense. Additionally, ferroptosis, characterized by mitochondrial damage and elevated Fe²⁺ levels, was reduced in RIN1 knockdown rats. Treatment with Nrf2 or HO-1 activators improved pain sensitivity and reduced inflammation, while inhibition of Nrf2 activity attenuated the protective effects of RIN1 silencing. <em>In vitro</em>, RIN1 silencing reduced activation LPS-treated of mouse BV2 microglial cells, leading to a decrease in the secretion of pro-inflammatory cytokines (IL-6, TNFα, and IL-1β), reduced microglial ferroptosis, and decreased the cytotoxicity of BV2 cells to co-cultured neurons. These effects were mediated by the Nrf2 pathway, as Nrf2 antagonism reversed the effects of RIN1 knockdown. These findings suggest that RIN1 plays a critical role in spinal cord hypersensitivity and pain perception by inhibiting the Nrf2/HO-1 pathway, influencing neuroinflammation and ferroptosis. Targeting RIN1 could provide a potential therapeutic strategy for managing NP and neuroinflammation.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111784"},"PeriodicalIF":4.4,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810664","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}

{"title":"Corrigendum to “CCR7/DUSP1 signaling axis mediates iCAF to regulate head and neck squamous cell carcinoma growth” [Cellular Signalling, October 2024, Volume 122, 111305]","authors":"Jiaxing Gao ,&nbsp;Zengxu Wang ,&nbsp;Shanfeng Lin ,&nbsp;Yuan Tian ,&nbsp;Haoxuan Wu ,&nbsp;Zhenning Li ,&nbsp;Fayu Liu","doi":"10.1016/j.cellsig.2025.111768","DOIUrl":"10.1016/j.cellsig.2025.111768","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"131 ","pages":"Article 111768"},"PeriodicalIF":4.4,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787924","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}

{"title":"Loureirin B analogs mitigate oxidative stress and confer renal protection","authors":"Haowen Fang ,&nbsp;Xiaodong Sun ,&nbsp;Yanting Ding ,&nbsp;Bing Niu ,&nbsp;Qin Chen","doi":"10.1016/j.cellsig.2025.111787","DOIUrl":"10.1016/j.cellsig.2025.111787","url":null,"abstract":"<div><div>Diabetic kidney disease (DKD) is a microvascular complication of diabetes with high morbidity and mortality, necessitating effective treatment. In this study, the Loureirin B analogue (LB-A) was utilized to treat DKD in mice. The results demonstrated that LB-A effectively prevent the progression of DKD in mice, significantly lowering fasting blood glucose levels and reducing proteinuria levels. Additionally, there was a significant decrease in oxidase content in the kidneys of mice, accompanied by an increase in antioxidant oxidase content, resulting in a decrease in ROS levels, mitigating oxidative stress state through modulation of Cxcl1. Cell experiments further confirmed that reducing Cxcl1/Cxcr2 axis activation prevented the onset of DKD induced by high glucose exposure and affected the therapeutic effect of LB-A as well. These findings provide evidences to support that LB-A may mitigate oxidative stress by modulating the Cxcl1 signaling pathway, thereby contributing to renal protection in the context of DKD treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111787"},"PeriodicalIF":4.4,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794710","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}

{"title":"Comprehensive evaluation of differential expression of piRNAs in abdominal aortic aneurysm","authors":"Xiaoxin Jiang ,&nbsp;Yajun Zhang ,&nbsp;Yuanyuan Li ,&nbsp;Xiaoqian Li ,&nbsp;Yanyan Yang ,&nbsp;Tao Yu","doi":"10.1016/j.cellsig.2025.111785","DOIUrl":"10.1016/j.cellsig.2025.111785","url":null,"abstract":"<div><div>Abdominal aortic aneurysm (AAA) is a prevalent and fatal cardiovascular condition characterized by a high incidence rate and nonspecific clinical manifestations, with no effective preventive or therapeutic measures currently available. Piwi-interacting RNAs (piRNAs) have been identified as significant biomarkers for disease diagnosis due to their essential functions in transposon suppression, maintenance of genomic stability, immune response, and epigenetic modulation. The piRNA is intimately associated with various diseases such as cardiac hypertrophy, tumors, and neurodegeneration, yet its role in AAA is unclear. In this study, we employed gene sequencing to analyze the piRNA expression profiles in AAA vascular tissues and predicted variations in their target genes. Our findings revealed a total of 1368 piRNAs with abnormal expression in the AAA group relative to the control group, including 1240 up-regulated and 128 down-regulated piRNAs (|log2(fold change)| ≥ 1.0), with 82 demonstrating significant differences (<em>P</em> &lt; 0.05). Through bioinformatics analysis, it was determined that the Wnt signaling pathway, calcium signaling, TNF-α and the p53 pathway are crucial mechanisms by which piRNAs contribute to the development of AAA. RT-qPCR confirmed that hsa_piR_011324 was the most significantly up-regulated piRNA in AAA (<em>P</em> &lt; 0.0001), corroborating RNA sequencing results. Further results indicate that hsa_piR_011324 promotes phenotypic transformation of human aortic vascular smooth muscle cells (HAVSMCs), enhances the activity of matrix metalloproteinases (MMPs), increased up-regulation of inflammation-related markers IL-1β and TNF-α, and induces apoptotic processes. In conclusion, the present study emphasizes the important regulatory role of hsa_piR_011324 in AAA, suggesting that it holds promise as a prospective target for diagnostic and therapeutic intervention.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111785"},"PeriodicalIF":4.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787923","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}

{"title":"The m6A RNA demethylase FTO promotes radioresistance and stemness maintenance of glioma stem cells","authors":"Junhao Zhang ,&nbsp;Guoxi Li ,&nbsp;Runqiu Wu ,&nbsp;Lin Shi ,&nbsp;Cong Tian ,&nbsp;Hongyan Jiang ,&nbsp;Hongyu Che ,&nbsp;Yongang Jiang ,&nbsp;Zhiyong Jin ,&nbsp;Rutong Yu ,&nbsp;Xuejiao Liu ,&nbsp;Xu Zhang","doi":"10.1016/j.cellsig.2025.111782","DOIUrl":"10.1016/j.cellsig.2025.111782","url":null,"abstract":"<div><div>Glioblastoma (GBM) was the most common and deadliest malignant brain tumor in adults, with a poor prognosis. Effective targeted drugs are still lacking, and the presence of glioblastoma stem cells (GSC) is a major factor contributing to radiotherapy resistance. Screening for targeted drugs that can sensitize GBM to radiotherapy is crucial. FTO is considered an attractive potential target for tumor therapy, as it mediates m6A demethylation to regulate the stability of target genes. In this study, we evaluated the role of FTO inhibition in promoting the sensitivity of GSC cells to radiotherapy through tumor sphere formation assays, cell apoptosis assays, and in situ GSC tumor models. We preliminarily explored the molecular mechanisms by transcriptome sequencing and m6A methylation sequencing to investigate how inhibiting FTO increases radiotherapy sensitivity. The results showed that downregulation of FTO expression or FTO inhibitor FB23-2 combined with radiotherapy significantly inhibited GSC cell proliferation and self-renewal and increased apoptosis. FB23-2 combined with radiotherapy effectively inhibited intracranial tumor growth in mice and prolonged the survival of tumor-bearing mice. Furthermore, FTO inhibition sustained the increase of γH2AX expression induced by radiotherapy while decreasing Rad51 expression. Importantly, we found that inhibiting FTO could increase m6A methylation modification of VEGFA, thereby downregulating both mRNA and protein expression of VEGFA. Our findings provide a new therapeutic strategy for enhancing GBM radiotherapy sensitivity and lay the theoretical and experimental groundwork for clinical trials targeting FTO.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"132 ","pages":"Article 111782"},"PeriodicalIF":4.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768635","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}