Cell Biology International最新文献_第3页

DRIM modulates Src activation and regulates angiogenic functions in vascular endothelial cells 在血管内皮细胞中，DRIM调节Src激活和血管生成功能。

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":"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":"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}

引用次数: 0

The potential role of the SIRT1-Nrf2 signaling pathway in alleviating hidden hearing loss via antioxidant stress SIRT1-Nrf2信号通路在通过抗氧化应激减轻隐性听力损失中的潜在作用。

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":"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":"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}

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":"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":"49 3","pages":"250-261"},"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":"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":"49 2","pages":"188-200"},"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

Correction to “The Hippo–YAP pathway regulates the proliferation of alveolar epithelial progenitors after acute lung injury” 对 "急性肺损伤后肺泡上皮祖细胞的增殖受 Hippo-YAP 通路调控 "的更正。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-06 DOI: 10.1002/cbin.12247

引用次数: 0

ZNF655 involved in the progression of multiple myeloma via the activation of AKT ZNF655 通过激活 AKT 参与多发性骨髓瘤的进展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-11-03 DOI: 10.1002/cbin.12256

Haiming Kou, Shuqin Jiang, Xueqiong Wu, Changhua Jing, Xinxin Xu, Jiaju Wang, Cui Zhang, Wenting Liu, Yan Gao, Qian Men, Ping Lu, Zhenhui Lv

{"title":"ZNF655 involved in the progression of multiple myeloma via the activation of AKT","authors":"Haiming Kou, Shuqin Jiang, Xueqiong Wu, Changhua Jing, Xinxin Xu, Jiaju Wang, Cui Zhang, Wenting Liu, Yan Gao, Qian Men, Ping Lu, Zhenhui Lv","doi":"10.1002/cbin.12256","DOIUrl":"10.1002/cbin.12256","url":null,"abstract":"Multiple myeloma (MM) is an incurable hematological malignancy, and the number of MM patients is increasing year by year. Zinc finger protein 655 (ZNF655) has been shown to regulate various biological processes and is implicated in the progression of many diseases. However, the roles of ZNF655 in MM progression remains unclear. In this study, we aimed to explore the effects of ZNF655 on progression by detecting the alteration of the phenotypes and tumorigenesis induced by ZNF655 knockdown in MM. The expression level of ZNF655 in MM was clarified by real-time quantitative polymerase chain reaction assays. Furthermore, loss-of-function assays in vitro and in vivo was investigated the biological functions of ZNF655 in MM. These findings revealed that ZNF655 depletion remarkably inhibited MM cell proliferation, arrested cell cycle, and induced cell apoptosis. Mechanistically, ZNF655 was found to regulate AKT in MM. In conclusion, this study indicated that ZNF655 regulated the progression of MM via AKT activation and downregulation of ZNF655 may be a promising antitumor strategy in MM.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"177-187"},"PeriodicalIF":3.3,"publicationDate":"2024-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567460","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

MARCHF1 promotes breast cancer through accelerating REST ubiquitylation and following TFAM transcription MARCHF1 通过加速 REST 泛素化和跟随 TFAM 转录来促进乳腺癌的发生。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-10-20 DOI: 10.1002/cbin.12255

Jutao Li, Zhenming Gao

{"title":"MARCHF1 promotes breast cancer through accelerating REST ubiquitylation and following TFAM transcription","authors":"Jutao Li, Zhenming Gao","doi":"10.1002/cbin.12255","DOIUrl":"10.1002/cbin.12255","url":null,"abstract":"Breast cancer has become the leading cause of death in women. Membrane associated ring-CH-type finger 1 (MARCHF1) is associated with the development of various types of cancer, but the exact role of MARCHF1 in breast cancer remains unclear. In our study, the higher MARCHF1 expression was observed in tumor samples of patients with breast cancer and then the role of MARCHF1 in breast cancer was further evaluated. Overexpression of MARCHF1 contributed to proliferation of cancer cells and inhibition of oxidative stress. Knockdown of MARCHF1 reduced breast cancer cell proliferation, increased mitochondrial dysfunction induced by oxidative stress, eventually aggravating cell death. In vivo, MARCHF1 promoted the tumor growth and oppositely, MARCHF1 silencing suppressed the tumor development. Moreover, MARCHF1 interacted with repressor Element-1 silencing transcription factor (REST) and facilitated its ubiquitylation and degradation. Subsequently, REST negatively regulated the transcription of mitochondrial transcription factor A (TFAM). The subcutaneous tumor formation assay in nude mice also supported these conclusions. In details, knockdown of MARCHF1 upregulated the protein expression of REST and downregulated the mRNA level of TFAM. On the contrary, MARCHF1 overexpression exhibited opposite effects. Thus, MARCHF1 is conducive to the progression of breast cancer via promoting the ubiquitylation and degradation of RSET and then the transcription of TFAM. Downregulating MARCHF1 could provide a novel direction for treating breast cancer.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 2","pages":"161-176"},"PeriodicalIF":3.3,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459183","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