Cell Biology International最新文献

Wilms' tumor 1-associated protein aggravates ischemic stroke by promoting M1 polarization of microglia by enhancing PTGS2 mRNA stability in an m6A-dependent manner.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-17 DOI: 10.1002/cbin.12266

Haijing Sui, Chang Liu, Zhenyu Sun, Hongjie Xi

{"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, Chang Liu, Zhenyu Sun, Hongjie Xi","doi":"10.1002/cbin.12266","DOIUrl":"https://doi.org/10.1002/cbin.12266","url":null,"abstract":"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.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoding dynamic molecular interactions in cells. 解码细胞中的动态分子相互作用。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-17 DOI: 10.1002/cbin.12262

Mussarat Rafiq, Chengcheng Hu, Xinjiao Gao, Zhikai Wang, Sergio Schenkman, Andreas Merdes, Xing Liu

引用次数: 0

Therapeutic targeting of cGAS-STING pathway in lung cancer.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-08 DOI: 10.1002/cbin.12263

Jinli Wang, Lumin Xing

{"title":"Therapeutic targeting of cGAS-STING pathway in lung cancer.","authors":"Jinli Wang, Lumin Xing","doi":"10.1002/cbin.12263","DOIUrl":"https://doi.org/10.1002/cbin.12263","url":null,"abstract":"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.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"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}

引用次数: 0

DRIM modulates Src activation and regulates angiogenic functions in vascular endothelial cells.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-08 DOI: 10.1002/cbin.12265

Jia Tong, Xuefei Dong, Tracey A Martin, Yiming Yang, Bo Dong, Wen G Jiang

{"title":"DRIM modulates Src activation and regulates angiogenic functions in vascular endothelial cells.","authors":"Jia Tong, Xuefei Dong, Tracey A Martin, Yiming Yang, Bo Dong, Wen G Jiang","doi":"10.1002/cbin.12265","DOIUrl":"https://doi.org/10.1002/cbin.12265","url":null,"abstract":"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.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The potential role of the SIRT1-Nrf2 signaling pathway in alleviating hidden hearing loss via antioxidant stress.

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-12-01 DOI: 10.1002/cbin.12264

Zeyu Zheng, Peng Zhang, Yang Fu, Yihong Jiang, Jing Zhu, Fei Wang, Shaoheng Li, Zhuoru Zhang, Tong Chang, Tian Li, Min Zhang, Bai Ruan, Xiaocheng Wang

{"title":"The potential role of the SIRT1-Nrf2 signaling pathway in alleviating hidden hearing loss via antioxidant stress.","authors":"Zeyu Zheng, Peng Zhang, Yang Fu, Yihong Jiang, Jing Zhu, Fei Wang, Shaoheng Li, Zhuoru Zhang, Tong Chang, Tian Li, Min Zhang, Bai Ruan, Xiaocheng Wang","doi":"10.1002/cbin.12264","DOIUrl":"https://doi.org/10.1002/cbin.12264","url":null,"abstract":"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.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Artesunate alleviates radiation-induced submandibular gland epithelial cell damage in rats by reducing inflammation and apoptosis. 青蒿琥酯可通过减少炎症和细胞凋亡减轻辐射引起的大鼠颌下腺上皮细胞损伤。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-28 DOI: 10.1002/cbin.12261

Yuchen Wang, Danni Zhao, Xiaolin Nong

{"title":"Artesunate alleviates radiation-induced submandibular gland epithelial cell damage in rats by reducing inflammation and apoptosis.","authors":"Yuchen Wang, Danni Zhao, Xiaolin Nong","doi":"10.1002/cbin.12261","DOIUrl":"https://doi.org/10.1002/cbin.12261","url":null,"abstract":"Salivary hypofunction is a common complication in patients with head and neck cancers following radiotherapy (RT). RT-induced inflammation in salivary gland cells leads to apoptosis and fibrosis. Artesunate (ART) is a bioactive compound with anti-inflammatory and anti-fibrosis properties. This study aimed to investigate the protective effects of ART on X-ray-induced injury of submandibular gland (SMG) epithelial cells in rats. Second-generation SMG epithelial cells were randomly divided into five groups: natural control group (NC), irradiated group (IR), and irradiated groups treated with ART at concentrations of 5, 10, and 20 μM. Cells were harvested 48 h postirradiation for analysis. The results demonstrated that ART attenuated the damage to AQP5, a crucial indicator of salivary gland function, as evidenced by the decreased expression of AQP5 at both mRNA and protein levels. Additionally, ART decreased the expression of inflammatory cytokines: IL-6 and TNF-α. TUNEL staining revealed reduced apoptosis in the ART groups, particularly the IR + 10 μM group. RT-PCR and Western blot analysis of apoptosis cytokines Bax/Bcl-2 and Caspase-3 confirmed these findings. Furthermore, ART inhibited the expression of NF-κB at both mRNA and protein levels. In conclusion, these results suggest that ART may reduce inflammation and apoptosis in SMG epithelial cells following radiation by inhibiting the NF-κB pathway.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738478","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}

引用次数: 0

Deciphering HMGB1: Across a spectrum of DNA and nucleosome dynamics. 解密 HMGB1：横跨 DNA 和核小体动力学谱系

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-17 DOI: 10.1002/cbin.12260

Ishu Gupta, Ashok K Patel

引用次数: 0

SSX2IP promotes cell proliferation and migration in breast cancer by regulating FANCI. SSX2IP 通过调节 FANCI 促进乳腺癌细胞的增殖和迁移。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-12 DOI: 10.1002/cbin.12259

Xianfu Liu, Xiaojing Zhang, Yansong Chen, Jingwei Tang, Hao Zhang, Gongsheng Jin

{"title":"SSX2IP promotes cell proliferation and migration in breast cancer by regulating FANCI.","authors":"Xianfu Liu, Xiaojing Zhang, Yansong Chen, Jingwei Tang, Hao Zhang, Gongsheng Jin","doi":"10.1002/cbin.12259","DOIUrl":"https://doi.org/10.1002/cbin.12259","url":null,"abstract":"Synovial sarcoma X breakpoint 2 interacting protein (SSX2IP) is expressed in various normal tissues and participates in the progression of human cancers. Nevertheless, the specific functions and underlying molecular mechanisms of SSX2IP in cancer, particularly in breast cancer, remain poorly understood. In this study, we aimed to explore the functional role of SSX2IP in breast cancer. Immunohistochemical staining, quantitative real-time PCR, and western blotting blot analysis were used to assess genes expression levels. By manipulating SSX2IP expression levels and conducting functional assays including Celigo cell counting assay or CCKCCK-8-8 assay, flow cytometry, wound healing assay, and Transwell assay, we explored the impact of SSX2IP on the malignant phenotype of breast cancer cells. Additionally, the in vivo tumor-suppressive ability of SSX2IP was investigated by tumor xenograft experiment. Our results revealed an upregulation of SSX2IP in the breast cancer. Functional assays demonstrated that SSX2IP knockdown inhibited cell proliferation and migration, induced apoptosis in vitro, as well as suppressed the tumor growth in vivo. Conversely, SSX2IP overexpression contributed to the malignant phenotype of breast cancer cells. Co-expression analysis showed that FA Complementation Group I (FANCI) was co-expressed with SSX2IP. Additionally, SSX2IP positively regulated FANCI expression and its interaction was verified by Co-IP.Co-IP. Furthermore, FANCI overexpression partially reversed the effects of SSX2IP knockdown on cell proliferation and metastasis. In summary, our findings revealed that SSX2IP contributes to the progression of breast cancer by regulating FANCI, hinting at its potential as a novel biomarker and therapeutic target for the treatment of breast cancer.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615452","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}

引用次数: 0

Involvement of PDGFR-integrin interactions in the regulation of anoikis resistance in glioblastoma progression 表皮生长因子受体-整合素相互作用参与调控胶质母细胞瘤进展过程中的阿诺伊克抗性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-10 DOI: 10.1002/cbin.12257

Pampa Pain, Ashutosh Tripathi, Prakash P. Pillai

{"title":"Involvement of PDGFR-integrin interactions in the regulation of anoikis resistance in glioblastoma progression","authors":"Pampa Pain, Ashutosh Tripathi, Prakash P. Pillai","doi":"10.1002/cbin.12257","DOIUrl":"10.1002/cbin.12257","url":null,"abstract":"The interactions between platelet-derived growth factor/PDGF receptor and integrin signaling are crucial for cells to respond to extracellular stimuli. Integrin interactions with PDGFR within the lipid rafts activate downstream cellular signaling pathways that regulate cell proliferation, cell migration, cell differentiation, and cell death processes. The mechanisms underlying PDGFR activation mediated receptor internalization, interactions with other cell-surface receptors, particularly extracellular matrix receptors, integrins, and how these cellular mechanisms switch on anchorage-independent cell survival, leading to anoikis resistance are discussed. The role of regulatory molecules such as noncoding RNAs, that can modulate several molecular and cellular processes, including autophagy, in the acquisition of anoikis resistance is also discussed. Overall, the review provides a new perspective on a complex interplay of regulatory cellular machineries involving autophagy, noncoding RNAs and cellular mechanisms of PDGFR activation, PDGFR-integrin interactions, and involvement of lipids rafts in the acquisition of anoikis resistance that regulates glioblastoma progression along with potential future strategies to develop novel therapeutics for glioblastoma multiforme.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 1","pages":"3-15"},"PeriodicalIF":3.3,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615449","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}

引用次数: 0

Carnosol alleviates cisplatin–induced acute kidney injury by regulating apoptosis and pyroptosis 卡诺索尔通过调节细胞凋亡和热解减轻顺铂诱导的急性肾损伤

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-10 DOI: 10.1002/cbin.12258

Chunjie Li, Hongyan Yang, Yuan Wu, Mingke Zhou, Hengbiao Luo, Peng Yuan, Fengge Shen

{"title":"Carnosol alleviates cisplatin–induced acute kidney injury by regulating apoptosis and pyroptosis","authors":"Chunjie Li, Hongyan Yang, Yuan Wu, Mingke Zhou, Hengbiao Luo, Peng Yuan, Fengge Shen","doi":"10.1002/cbin.12258","DOIUrl":"10.1002/cbin.12258","url":null,"abstract":"The use of the common anticancer drug cisplatin (CP) in clinical practice often leads to acute kidney injury (AKI); however, no protective therapy is available. Therefore, new drugs that reduce the nephrotoxicity induced by CP are urgently needed. Carnosol (CA) is an antioxidant found. We investigated the renoprotective effects of CA on CP-induced AKI in male C57BL/6 mice and HK2 cells. CA mitigated renal dysfunction, histopathological changes and tubular injury in vivo, as indicated by the expression of NGAL, KIM1 and HMGB1. Moreover, the numbers of apoptotic cells and the expression of apoptotic proteins were dramatically reduced after CA treatment in mouse kidneys and HK2 cells. CA significantly ameliorated CP-induced inflammation and decreased TNF-α and IL-1β levels in vivo and in vitro and macrophage infiltration in the mouse kidney. CA decreased the expression levels of p-p65/p65, NLRP3 and ASC, which indicates that CA suppressed the activation of the NF-κB/NLRP3 signaling axis induced by CP in vivo and in vitro. In addition, CA decreased the levels of certain protein in pyroptotic cells, as indicated by the expression of cleaved caspase-1, GSDMD, and mature IL-1β and IL-18 in vivo and in vitro. Finally, CA reduced the level of cleaved caspase-1, but those of GSDMD and NLRP3 protein were not significantly different after treatment with the NLRP3 inhibitor MCC950 and were elevated by the NLRP3 activator nigericin. In conclusion, this study revealed that CA protects against CP-induced AKI by decreasing apoptosis and NF-κB/NLRP3/GSDMD-mediated pyroptosis, which provides new insight into the prevention of AKI.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 1","pages":"101-117"},"PeriodicalIF":3.3,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615430","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}

引用次数: 0