Cell Biology International最新文献

{"title":"Glucuronoxylomannan (GXM) modulates macrophage proliferation and apoptosis through the STAT1 signaling pathway","authors":"Youming Huang,&nbsp;Sujing Li,&nbsp;Yan Teng,&nbsp;Xiaoxia Ding,&nbsp;Danfeng Xu,&nbsp;Xianhong Yang,&nbsp;Yong Yu,&nbsp;Yibin Fan","doi":"10.1002/cbin.12267","DOIUrl":"10.1002/cbin.12267","url":null,"abstract":"<p><i>cryptococcus neoformans</i> (<i>C. neoformans</i>) is a crucial opportunistic fungus that possesses an encapsulated fungal pathogen. The cryptococcal capsule is mainly composed of the polysaccharide glucuronoxylomannan (GXM). Macrophages form the first-line innate defense against cryptococcosis; however, the underlying mechanism remains unclear. In this study, GXM-treated RAW264.7 macrophages showed a notably reduced survival rate and increased apoptosis, accompanied by the promoted inducible nitric oxide synthase (iNOS) expression and NO production. Signal transducer and activator of transcription 1 (STAT1) expression was also found to be directly proportional to GXM concentration; STAT1 knockdown could alleviate GXM-induced proliferation decrease and apoptosis increase of macrophages, as well as reduce M1 polarization, iNOS expression and NO release. In conclusion, this study concluded that GXM was the main virulence factor of <i>C. neoformans</i>, which is critical in determining the mechanism of GXM-mediated protective immune response postinfection. The STAT1 signal pathway mediates the effect of GXM stimulation on macrophages, potentially providing a reference for further understanding the biological role of GXM.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"317-328"},"PeriodicalIF":3.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930802","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}

{"title":"RETRACTION: GANT61 Plays Antitumor Effects by Inducing Oxidative Stress through the miRNA-1286/RAB31 Axis in Osteosarcoma","authors":"","doi":"10.1002/cbin.12271","DOIUrl":"10.1002/cbin.12271","url":null,"abstract":"<p><b>RETRACTION:</b> K.-q. Zhang, X.-d. Chu, “GANT61 Plays Antitumor Effects by Inducing Oxidative Stress through the miRNA-1286/RAB31 Axis in Osteosarcoma,” <i>Cell Biology International</i> 45, no. 1 (2020): 61–73, https://doi.org/10.1002/cbin.11467.</p><p>The above article, published online on 16 September 2020, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Xuebiao Yao; and John Wiley &amp; Sons Ltd.  A third party notified the publisher that this article had reused images that had been used in multiple different publications, each by different sets of authors.</p><p>Specifically, images from this article have been re-used from the following publications which had published before or near the same time: (Lei, et al. 2020 [https://doi.org/10.2147/OTT.S214514]); (Sun, et al. 2020 [https://doi.org/10.1002/cam4.2723]); (Hu, et al. 2020 [https://doi.org/10.2147/CMAR.S260693]); (Zhao, et al. 2020 [https://doi.org/10.21037/atm-20-5586]); (Ma, et al. 2020 [https://doi.org/10.21037/tcr.2020.04.13]); (Hong, et al. 2020 [https://doi.org/10.18632/aging.103278]); (Chen, et al. 2020 [https://doi.org/10.1002/cam4.2839]); (Wu, et al. 2019 [https://doi.org/10.3233/cbm-190534]); (Chen, et al. 2020 [https://doi.org/10.21037/tcr-20-940]); (Kang, et al. 2020 [https://doi.org/10.21037/tcr-20-1727]); (Wei, et al. 2020 [https://doi.org/10.2147/DDDT.S222694]); and (Xie, et al. 2020 [https://doi.org/10.21037/atm-20-7201]).</p><p>In addition, images that appeared in this article have also been detected in the following subsequent publications: (Zhang &amp; Song 2020 [https://doi.org/10.21037/atm-20-7253]); (Qiao, et al. 2021 [https://doi.org/10.1186/s12885-021-08730-7]); (Lv, et al. 2022 [https://doi.org/10.1080/13880209.2022.2032206]); (Yao, et al. 2022 [https://doi.org/10.1080/21655979.2022.2060776]); and (Zhou, et al. 2021 [https://doi.org/10.21037/atm-20-7365]). The authors did not respond to inquiries by the publisher. The retraction has been agreed to because the evidence of image duplications across different articles, each of which reports on different experimental conditions, fundamentally compromises the conclusions of this article. The authors did not respond to our notice regarding the retraction.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"201"},"PeriodicalIF":3.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913496","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}

{"title":"Melatonin promotes the proliferation and differentiation of antler chondrocytes via RUNX2 dependent on the interaction between NOTCH1 and SHH signaling pathways","authors":"Qiaoling Zhang,&nbsp;Yan Zhang,&nbsp;Baiyu Li,&nbsp;Chenhao Wang,&nbsp;Zhanqing Yang,&nbsp;Bin Guo,&nbsp;Zhanpeng Yue","doi":"10.1002/cbin.12272","DOIUrl":"10.1002/cbin.12272","url":null,"abstract":"<p>Melatonin (MT), an endogenous hormone secreted by pineal gland, has the sedative, anti-inflammatory and antioxidant functions. However, there are few studies on whether MT affects the proliferation and differentiation of antler chondrocytes. The present study investigated the influences of MT on the proliferation and differentiation of antler chondrocytes, explored its regulation on runt-related transcription factor 2 (RUNX2), NOTCH1 and sonic hedgehog (SHH) signaling, and elucidated their interplays. The results showed that MT promoted the proliferation of antler chondrocytes and induced the differentiation of chondrocytes into hypertrophic chondrocytes as evidenced by the significant increase of collagen type X (<i>COL X</i>), alkaline phosphatase (<i>ALP</i>) and matrix metalloproteinase 13 (<i>MMP13</i>) expression and ALP activity, the well-established markers for hypertrophic chondrocytes, but this effectiveness was neutralized by the addition of MT receptor antagonist. Further analysis indicated that MT activated the NOTCH1 and SHH signaling whose blockage abrogated the inducement of MT on the proliferation and differentiation of antler chondrocytes. SHH was identified as a downstream target of recombination signal binding protein for immunoglobulin kappa J region (RBPJ), a transcription factor of NOTCH1 signaling. Meanwhile, MT stimulated the expression of <i>RUNX2</i> through activating the SHH signaling whose downstream transcription factor glioma-associated oncogene 1 (GLI1) directly controlled the transcription of <i>RUNX2</i> through binding to its promoter region. Moreover, repression of GLI1 counteracted the proliferative effect of MT on antler chondrocytes and attenuated the advancement of MT on chondrocyte differentiation, while supplementation of recombinant RUNX2 protein recued above effects. Collectively, MT induced the proliferation and differentiation of antler chondrocytes via RUNX2 dependent on the interaction between NOTCH1 and SHH signaling pathways.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"329-342"},"PeriodicalIF":3.3,"publicationDate":"2024-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906359","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}

{"title":"Calcium level and autophagy defect in GNE mutants of rare neuromuscular disorder","authors":"Shweta Sharma,&nbsp;Fluencephila Mashangva,&nbsp;Jyoti Oswalia,&nbsp;Shagun Singh,&nbsp;Rohan Alag,&nbsp;Ranjana Arya","doi":"10.1002/cbin.12268","DOIUrl":"10.1002/cbin.12268","url":null,"abstract":"<p>Rare genetic disorders are low in prevalence and hence there is little or no attention paid to them in the mainstream medical industry. One of the ultra-rare neuromuscular disorders, GNE myopathy is caused due to biallelic mutations in the bifunctional enzyme, GNE (UDP N-acetylglucosamine-2-epimerase/N-acetylmannosamine kinase). It catalyses the rate-limiting step in sialic acid biosynthesis. There are no effective treatments for GNE myopathy as the pathomechanism is poorly understood. Pathologically, the disease is characterized by the formation of rimmed vacuoles that contain aggregates of β-amyloid, tau, presenilin etc proteins in muscle biopsy samples. Accumulation of aggregated proteins in the cells may occur due to the failure of the regulated autophagy phenomenon. In the present study, we aim to understand the effect of GNE mutations on autophagy. The cytosolic calcium levels in GNE mutant cells were found to be altered in a GNE mutation-specific manner. The chaperone levels, such as HSP70 and PDI, as well as autophagic markers (LC3II/I ratios) were altered in the GNE mutant cells. Treatment with BAPTA-AM, calcium chelator, significantly restored cytosolic calcium levels in some GNE mutant cells as well as autophagic marker levels and autophagic punctae formation. The effect on the calcium signalling cascade involving CaMKKβ/AMPK/mTOR was studied in the GNE mutant cells. Our study provides insights into the role of calcium in autophagic vacuole formation in the cells with GNE mutations that will have significance towards understanding the pathomechanism of GNE Myopathy and drug target identification for the rare disease.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 4","pages":"343-356"},"PeriodicalIF":3.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871531","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}

{"title":"Wnt/β-catenin pathway as a link between therapy resistance-driven epithelial-mesenchymal transition and stemness in colorectal cancer","authors":"Murilo Ramos Rocha,&nbsp;Yuri Kelly Castillo-Medina,&nbsp;Bárbara Martins de Lima Coelho,&nbsp;Luidy Lucas Lopes Rios,&nbsp;Jose Andres Morgado-Diaz","doi":"10.1002/cbin.12270","DOIUrl":"10.1002/cbin.12270","url":null,"abstract":"<p>The high plasticity of cells undergoing epithelial-mesenchymal transition (EMT) promotes increased tumor heterogeneity, and its interaction with tumor-associated stromal cells appears to contribute to developing a stemness phenotype. Cells with these characteristics exhibit increased resistance to chemotherapy and radiotherapy, leading to disease relapse and metastasis. Here, we discuss the activation of the Wnt/β-catenin pathway in promoting EMT and stemness within the context of cellular resistance to these therapies. We discuss whether EMT and cancer stem cells (CSCs) function in conjunction, independently, or if a link is connecting their development. We further propose that this pathway is necessary to establish a connection between these two phenotypes. And suggest that it could hinder the rise of CSCs from treatment-induced EMT cells when inhibited. Understanding this cellular phenomenon might allow the development of new targeted therapies to improve clinical responses, particularly in colorectal cancer.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"154-160"},"PeriodicalIF":3.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871533","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}

{"title":"Wilms' tumor 1-associated protein aggravates ischemic stroke by promoting M1 polarization of microglia by enhancing PTGS2 mRNA stability in an m6A-dependent manner","authors":"Haijing Sui,&nbsp;Chang Liu,&nbsp;Zhenyu Sun,&nbsp;Hongjie Xi","doi":"10.1002/cbin.12266","DOIUrl":"10.1002/cbin.12266","url":null,"abstract":"<p>Mounting evidence indicates the involvement of N6-methyladenosine (m6A) alterations in diverse neurological disorders and the activation of microglia. However, the role of m6A methyltransferase Wilms' tumor 1-associated protein (WTAP) in regulating microglial polarization during ischemic stroke (IS) remains unknown. We performed bioinformatics analysis to identify m6A-related differentially expressed genes in IS and validated these genes in a mouse middle cerebral artery occlusion model and a BV2 cell oxygen-glucose deprivation/reperfusion model. We found that microglial m6A modification was increased, and that WTAP was the most significantly differentially expressed m6A regulator during IS. High expression of WTAP is closely correlated with microglia-mediated neuroinflammation in IS. Mechanistically, WTAP promoted m6A modification, which promoted prostaglandin endoperoxide synthase-2 (PTGS2) by enhancing its mRNA stability. WTAP promoted M1 microglial polarization by elevating PTGS2 expression via m6A modification of PTGS2 mRNA in the oxygen-glucose deprivation/reperfusion model. In conclusion, WTAP is a crucial posttranscriptional regulator that contributes to post-IS neuroinflammation. WTAP knockdown confers cerebral protection by shifting the microglial phenotype from M1 to M2, primarily by reducing PTGS2 mRNA stability in an m6A-dependent manner.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 3","pages":"288-302"},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12266","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834281","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}

{"title":"Decoding dynamic molecular interactions in cells","authors":"Mussarat Rafiq,&nbsp;Chengcheng Hu,&nbsp;Xinjiao Gao,&nbsp;Zhikai Wang,&nbsp;Sergio Schenkman,&nbsp;Andreas Merdes,&nbsp;Xing Liu","doi":"10.1002/cbin.12262","DOIUrl":"10.1002/cbin.12262","url":null,"abstract":"","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"121-128"},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834280","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}

{"title":"Therapeutic targeting of cGAS–STING pathway in lung cancer","authors":"Jinli Wang,&nbsp;Lumin Xing","doi":"10.1002/cbin.12263","DOIUrl":"10.1002/cbin.12263","url":null,"abstract":"<p>The presence of DNA in the cytosol triggers a protective response from the innate immune system. Cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS–STING) is an essential cytosolic DNA sensor that triggers a potent innate immune response. As a result of this signaling cascade reaction, type I interferon and other immune mediators activate an immune response. The cGAS–STING pathway has great anticancer immunity-boosting potential since it produces type I interferons. The detection of double-stranded DNA (dsDNA) in response to various stimuli initiates a protective host's cGAS–STING signals. So, it is clear that a substantial relationship is expected between cancer biotherapy and the functioning of the cGAS–STING pathway. Several STING agonists with promising outcomes have been created for preclinical cancer therapy research. Notably, immunotherapy has dramatically extended patient survival and radically altered the course of lung cancer treatment, particularly in more advanced instances. However, this method is still ineffective for a large number of lung cancer patients. cGAS–STING can overcome resistance and boost anticancer immunity by stimulating the activity of many pro-inflammatory mediators, augmenting dendritic cell cross-presentation, and initiating a tumor-specific CD8⁺ T cell response. This review aims to present the most recent results on the functionality of the cGAS–STING pathway in cancer progression and its potential as an immunotherapy target, with a focus on lung cancer.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"129-138"},"PeriodicalIF":3.3,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794519","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}

{"title":"DRIM modulates Src activation and regulates angiogenic functions in vascular endothelial cells","authors":"Jia Tong,&nbsp;Xuefei Dong,&nbsp;Tracey A. Martin,&nbsp;Yiming Yang,&nbsp;Bo Dong,&nbsp;Wen G. Jiang","doi":"10.1002/cbin.12265","DOIUrl":"10.1002/cbin.12265","url":null,"abstract":"<p>Downregulated in Metastasis Protein (DRIM) was discovered in malignant epithelial cells and was thought to be mainly a nucleus protein affecting cancer cells. Recent single-cell sequencing analysis suggests that DRIM is abundantly expressed in vascular endothelial cells. There has been no knowledge of the role of DRIM in the endothelium. In the present study, using protein fraction method and cell imaging, we identified that the DRIM protein was abundantly present in both nucleus and the cytoskeletal fractions of human vascular endothelial cells. Knockdown of DRIM in the endothelial cells significantly affected growth, migration, and angiogenic tubule formation. Proteomics analyses revealed that Src was an important direct target protein of DRIM, a finding further confirmed by protein interaction assay. Silencing DRIM activated the tyrosine 419 site phosphorylation of Src kinase in endothelial cells, thereby affecting the downstream proteins of Src including p-FAK and p-STAT3, and exerting biological effects. To conclude, our results provide evidence of DRIM being a nuclear and cytoskeletal-associated protein, having a novel key role of the protein in vascular endothelial cells.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 3","pages":"277-287"},"PeriodicalIF":3.3,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12265","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794517","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}

{"title":"The potential role of the SIRT1-Nrf2 signaling pathway in alleviating hidden hearing loss via antioxidant stress","authors":"Zeyu Zheng,&nbsp;Peng Zhang,&nbsp;Yang Fu,&nbsp;Yihong Jiang,&nbsp;Jing Zhu,&nbsp;Fei Wang,&nbsp;Shaoheng Li,&nbsp;Zhuoru Zhang,&nbsp;Tong Chang,&nbsp;Tian Li,&nbsp;Min Zhang,&nbsp;Bai Ruan,&nbsp;Xiaocheng Wang","doi":"10.1002/cbin.12264","DOIUrl":"10.1002/cbin.12264","url":null,"abstract":"<p>Hidden hearing loss (HHL) is characterized by normal audiometric thresholds but impaired auditory function, particularly in noisy environments. In vivo, we employed auditory brainstem response (ABR) testing and ribbon synapses counting to assess changes in mouse hearing function, and observed the morphology of hair cells through scanning electron microscopy. SRT1720 was administered to the cochlea via round window injection. In vitro, western blot analysis and RT-qPCR were used, and Lenti-shNrf2 was used to knockdown Nrf2 expression. In addition, various oxidative stress indicators were detected by immunofluorescence, kit-based assays, and flow cytometry. ABR measurement of HHL mouse showed a significant increase in hearing threshold, as well as a decrease and delay in the I wave amplitude and latency on the first day after noise exposure. Histological observation showed a significant loss of ribbon synapses and stereocilia lodging. HHL mice exhibited oxidative stress, which was reduced by pretreatment with SRT1720. Additionally, SRT1720 could reduce hydrogen peroxide-induced oxidative stress in HEI-OC1 cells through activating the SIRT1/Nrf2 pathway. Subsequent experiments with Nrf2 knockdown confirmed the importance of this pathway. findings highlight oxidative stress as the primary contributor to HHL, with the SIRT1/Nrf2 signaling pathway emerging as a promising therapeutic target for alleviating HHL.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 3","pages":"262-276"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12264","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766718","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}