Cell Biology International最新文献_第3页

From Spheroid to Sprouting: Microenvironmental Modulation Boosts Hair Follicle Organoid Morphogenesis in 3D Culture 从球形到发芽：微环境调节促进毛囊类器官形态发生在三维培养。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-04 DOI: 10.1002/cbin.70045

Ling Xiao, Yunfan Tang, Feifei Zhang, Jiaping Zhang

{"title":"From Spheroid to Sprouting: Microenvironmental Modulation Boosts Hair Follicle Organoid Morphogenesis in 3D Culture","authors":"Ling Xiao, Yunfan Tang, Feifei Zhang, Jiaping Zhang","doi":"10.1002/cbin.70045","DOIUrl":"10.1002/cbin.70045","url":null,"abstract":"<div>\u0000 \u0000 Alopecia represents a global therapeutic challenge, with the challenge of achieving de novo folliculogenesis in alopecic regions rather than reactivating telogen-phase hair follicles to enhance hair density. The successful in vitro cultivation of hair follicle organoids (HFOs) and the effective enhancement of HFOs sprouting rates are critical advancements in addressing this problem. While R-spondin1 (RSPO1) demonstrates in vivo efficacy in activating quiescent follicular stem cells and enhancing hair density, its capacity to augment HFOs sprouting efficiency remains to be elucidated. In this study, we regulate the growth microenvironment of HFOs using RSPO1, enhancing the HFOs sprouting rate and exploring its mechanism. HFO-induced dermal papilla cells (DPCs) induction was quantified via alkaline phosphatase (ALP) assay, with RSPO1-mediated hair-regenerative gene/protein modulation assessed through triple-method analysis (qPCR/WB/IF). Sequencing delineated RSPO1-affected molecular pathways. Our study demonstrates that RSPO1 significantly promotes HFOs sprouting rate and upregulates the gene/protein expression of DPCs. Furthermore, RSPO1 not only potentiates Wnt/β-catenin-mediated organoid patterning but also coordinates a signaling triad involving PI3K-Akt, Rap1 and NF-κB to drive synchronized hair follicle sprouting and stratified pilogenic differentiation. Our 3D organoid-based expansion strategy enables definitive treatment of alopecia through in vitro hair follicle expansion, achieving functional hair neogenesis in patients with baldness.</div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"939-951"},"PeriodicalIF":3.3,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215045","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 “Effects of Syndecan-4 Silencing on the Extracellular Matrix Remodeling in Anoikis-Resistant Endothelial Cell” 修正“Syndecan-4沉默对抗抑郁内皮细胞细胞外基质重塑的影响”。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-04 DOI: 10.1002/cbin.70046

{"title":"Correction to “Effects of Syndecan-4 Silencing on the Extracellular Matrix Remodeling in Anoikis-Resistant Endothelial Cell”","authors":"","doi":"10.1002/cbin.70046","DOIUrl":"10.1002/cbin.70046","url":null,"abstract":"Onyeisi, J. O. S., H. B. Nader, and C. C. Lopes. 2024. “Effects of Syndecan-4 Silencing on the Extracellular Matrix Remodeling in Anoikis-Resistant Endothelial Cells.” Cell Biology International 48, no. 6: 883–897. https://doi.org/10.1002/cbin.12158.Following the publication of this article, the authors identified an error in Figure 4c. Specifically, the immunofluorescence image representing collagen IV expression in Adh1-EC cells was inadvertently replaced with a duplicate of the image for miR-Syn4-1-Adh1-EC cells. This error occurred during the final assembly of the figure and was unfortunately not detected before publication. A revised version of Figure 4c is provided below. This correction pertains solely to the visual presentation of immunofluorescence data in Figure 4c. It does not affect the results or conclusions of the study. Importantly, the quantification of collagen IV protein expression was based on western blot analysis (shown in Figure 4b), which remains accurate and unchanged.The authors sincerely apologize for this oversight and for any confusion, it may have caused. We remain committed to scientific transparency and integrity and are available to provide any additional supporting materials as needed.We apologize for this error and reaffirm our commitment to scientific integrity and transparency.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"1056-1057"},"PeriodicalIF":3.3,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215044","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

Trypanosoma Cruzi G and Y Strains' Metacyclic Trypomastigote Sheds Extracellular Vesicles and Trigger Host-Cell Communication. 克氏锥虫G株和Y株的超环锥马鞭毛虫脱落胞外囊泡并触发宿主-细胞通讯。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-02 DOI: 10.1002/cbin.70043

Paula Meneghetti, Ewa Kozela, Daniel Alfandari, Paula Abou Karam, Ziv Porat, Patricia Xander, Neta Regev-Rudzki, Sergio Schenkman, Ana Claudia Torrecilhas

{"title":"Trypanosoma Cruzi G and Y Strains' Metacyclic Trypomastigote Sheds Extracellular Vesicles and Trigger Host-Cell Communication.","authors":"Paula Meneghetti, Ewa Kozela, Daniel Alfandari, Paula Abou Karam, Ziv Porat, Patricia Xander, Neta Regev-Rudzki, Sergio Schenkman, Ana Claudia Torrecilhas","doi":"10.1002/cbin.70043","DOIUrl":"https://doi.org/10.1002/cbin.70043","url":null,"abstract":"Trypanosoma cruzi, a protozoan parasite, spontaneously releases extracellular vesicles (EVs) that facilitate communication with both invertebrate and vertebrate hosts. The results obtained by several groups indicated compositional variations in EVs generated by distinct types of T. cruzi. Nonetheless, few studies have characterized EVs derived from metacyclic trypomastigotes (MT), the form that develops in the vector and infects vertebrate hosts. This study aimed to characterize and compare EVs extracted from MTs of two T. cruzi parasite strains belonging to distinct groups with varying infectivity patterns. We examined the nature of these EVs and their influence on parasite-host interactions and host immune responses. Our findings demonstrated that EVs from G and Y strains showed no significant size differences; nonetheless, they exhibited variations in protein composition as shown by proteomic analysis, atomic force microscopy, and immunoenzymatic assays, including alterations in the presence of virulence factors. EVs from both strains interacted with and were taken up by human THP-1 monocytes, resulting in NF-κB activation. The EVs release from Y strain increase in the mRNA levels of RANTES, TNF-alpha, and IFN-beta, while inducing a similar nitric oxide (NO) increase relative to control cells. EVs from both strains also increased host cell invasion, however, EVs from the Y further increased the number of intracellular parasites. These results suggest that the infectivity of various strains by insect-derived forms correlates with EV secretion via the control of the host immune response, potentially leading to distinct infection patterns.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198321","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

Cancer Classification Through p53 Hotspot Mutations: An Ensemble Learning Approach. 通过p53热点突变进行癌症分类：一种集成学习方法。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-30 DOI: 10.1002/cbin.70041

Manisha R Patil, Anand Bihari

{"title":"Cancer Classification Through p53 Hotspot Mutations: An Ensemble Learning Approach.","authors":"Manisha R Patil, Anand Bihari","doi":"10.1002/cbin.70041","DOIUrl":"https://doi.org/10.1002/cbin.70041","url":null,"abstract":"Tumor suppressor protein p53 is attracting a lot of attention in cancer research because of its role in both tumor cell survival and apoptosis. The most frequently altered tumor suppressor gene in human cancer is TP53. TP53 mutations affecting residues in the protein's DNA binding domain (102-292) account for 80% of the alterations detected in tumors. These are called hotspot mutations because they lose their wild-type function and acquire oncogenic functions that accelerate cancer progression. These functions include promoting the growth, migration, invasion, and initiation of cancer cells and granting drug resistance to cancer cells. Six residues of the p53 protein (Arg175, Gly245, Arg249, Arg248, Arg273, and Arg282) are often altered in human cancer, known as hotspot mutations. Based on these hotspot codons, we identified the cancer types and stability of protein p53 in this study. This study aims to classify cancer types with a high degree of accuracy and precision. The main contribution of this study is that our work presented mutation data (clinically and biologically meaningful features and the role of hotspot codon of protein p53) to classify types of cancer by learning from the labeled data using an ensemble approach. Our research on the classification of cancer types outperformed using the Extreme Gradient boosting classifier (XGBoost) with an accuracy of 99.85%, precision of 99.80%, area under the curve of 100%, MCC of 99. 85%, and F1 of 99.80%.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181010","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

Harnessing Stem Cells for Pediatric Respiratory Diseases: Potential and Clinical Translation 利用干细胞治疗儿科呼吸系统疾病：潜力和临床转化。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-30 DOI: 10.1002/cbin.70042

Fatemeh Alizadeh, Sanaz Yasrebinia

引用次数: 0

Berberine Enhances the Sensitivity of Colorectal Cancer Cells to 5-FU Through Smoothing Endoplasmic Reticulum Stress-Mediated Autophagic Flux 小檗碱通过平滑内质网应激介导的自噬通量增强结直肠癌细胞对5-FU的敏感性

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-30 DOI: 10.1002/cbin.70038

Junyu Xu, Min Hu, Ying Li, Huiming Gong, Xiaoyan Zhang, Ziyue He, Chi Xiao, Chengzhong Yang, Jun Zeng

{"title":"Berberine Enhances the Sensitivity of Colorectal Cancer Cells to 5-FU Through Smoothing Endoplasmic Reticulum Stress-Mediated Autophagic Flux","authors":"Junyu Xu, Min Hu, Ying Li, Huiming Gong, Xiaoyan Zhang, Ziyue He, Chi Xiao, Chengzhong Yang, Jun Zeng","doi":"10.1002/cbin.70038","DOIUrl":"10.1002/cbin.70038","url":null,"abstract":"<div>\u0000 \u0000 Berberine (BBR), one of the main active isoquinoline alkaloids in Coptis chinensis, has gradually gained attention for its therapeutic effect on various tumors, including colorectal cancer (CRC). However, the detailed mechanisms underlying remain to be elucidated. The cytotoxic potential of BBR towards CRC cells was examined by MTT. Autophagy was indicated by acidic vesicular organelle formation, LC3 dots accumulation and conversion of LC3I to LC3II, while autophagic flux was monitored by the fusion of autophagosomes and lysosomes based on green fluorescence quenching in cells transfected with mRFP-GFP-LC3 plasmids and P62 degration. Furthermore, endoplasmic reticulum (ER) stress response-associated proteins in CRC cell lines treated with BBR and/or ER stress inhibitor 4-Phenylbutyric acid (4-BPA) were assessed by Western blotting. BBR-induced intracellular ROS accumulation was measured by DCFH-DA. ZIP Synergy scores were calculated using Synergyfinder software to evaluate the synergistic effects of BBR and 5-fluorouracil (5-FU). BBR induced cell death by autophagy-dependent mechanisms and resulted in sustained ER stress and oxidative stress, which contributed to the induction of complete autophagic flux. The inhibition of autophagy by chloroquine (CQ) partially reversed the anticancer effect of BBR, suggesting that BBR induced cytotoxic autophagy. Importantly, BBR enhanced the sensitivity of CRC cells to 5-FU.BBR might be a novel chemotherapy adjuvant drug that targets colorectal cancer by regulating ER stress/oxidative stress/autophagy/apoptosis.</div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"1042-1055"},"PeriodicalIF":3.3,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180848","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

Disruption of Retriever Function Impacts Retrograde Trafficking From Endosomes 寻回功能的破坏影响内体的逆行运输。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-29 DOI: 10.1002/cbin.70037

Zebin Li, Zhe Yang, Rohan D. Teasdale

{"title":"Disruption of Retriever Function Impacts Retrograde Trafficking From Endosomes","authors":"Zebin Li, Zhe Yang, Rohan D. Teasdale","doi":"10.1002/cbin.70037","DOIUrl":"10.1002/cbin.70037","url":null,"abstract":"Within endosomes cargo proteins are sorted and packaged into endosomal-transport carriers (ETCs) enabling their delivery to other intracellular compartments. Retromer, a conserved multimeric protein complex, has defined functions in sorting cargo mediating formation of ETCs for both retrograde trafficking back to the trans-Golgi network (TGN) and recycling of cargo to the cell surface. Recent studies have identified the retriever complex, which is structurally like retromer, that also can function in the recycling of cargo from endosomes. However, retriever's function in retrograde trafficking from endosomes has not been investigated. CrispR mediated knock-out cell models for retromer and retriever in A549 lung carcinoma epithelial cells were generated. Retriever's role in recycling of established cargo Integrin β1 in A549 cells was confirmed. Cation-independent mannose 6-phosphate receptor and TGN46, two well-established retrograde cargos showed a redistribution from the TGN to early endosomes in retromer knockout (KO) and retriever KO cells which is consistent with decreased retrograde trafficking. Application of a ETC redirection assay in A549 cells identified that ETCs dependent on either retromer or retriever can be tethered by Golgin97 and Golgin245, but not GCC88. Overall, the presence of retriever is required for efficient endosomal retrograde trafficking. Within A549 cells, the requirement of retromer for Wiskott-Aldrich Syndrome Protein and SCAR Homolog (WASH) endosomal recruitment was confirmed while recruitment of WASH in the absence of retriever was not reduced. Furthermore, the efficient recruitment of retriever to endosomes was dependent on retromer. The underlying mechanism by which these complexes initiate the formation of retrograde ETCs therefore seems distinct.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"1029-1041"},"PeriodicalIF":3.3,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172931","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

Flavokawain A Attenuated Chronic Kidney Disease: Evidence From Network Pharmacology and Experimental Verification 黄卡温A减毒慢性肾病：来自网络药理学和实验验证的证据。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-26 DOI: 10.1002/cbin.70036

Yugant Krishnakumar Talati, Neha Dagar, Anil Bhanudas Gaikwad

{"title":"Flavokawain A Attenuated Chronic Kidney Disease: Evidence From Network Pharmacology and Experimental Verification","authors":"Yugant Krishnakumar Talati, Neha Dagar, Anil Bhanudas Gaikwad","doi":"10.1002/cbin.70036","DOIUrl":"10.1002/cbin.70036","url":null,"abstract":"<div>\u0000 \u0000 Chronic kidney disease (CKD) is a silent global epidemic affecting ~700 million people worldwide, contributing to rising mortality rates. Despite the variety of underlying causes, renal fibrosis is the key pathological feature of CKD. Flavokawain A (FKA), a natural chalcone, is thought to offer protective effects against CKD through its anti-inflammatory, antioxidant, and anti-fibrotic properties. This study aims to investigate the therapeutic potential of FKA against CKD, using network pharmacology (NP), molecular docking analysis, and In Vivo validation. GeneCards, SwissTargetPrediction, and SuperPred databases were utilized to identify therapeutic targets related to CKD and FKA. Protein–protein interactions (PPIs) were performed using the STRING database. Gene ontology and pathway enrichment analyses were performed with DAVID databases, followed by network construction in Cytoscape. For validation, molecular docking studies were performed using PyRx and tested at doses of 50 mg/kg and 100 mg/kg (p.o.) for 21 days using a unilateral ureteral obstruction (UUO) rat model. The study identified 109 therapeutic targets for FKA in relation to CKD, highlighting 11 hub targets and 78 potential pathways. Molecular docking showed strong binding efficacy with nuclear factor κB subunit 1 (NF-κB1) and matrix metallopeptidase 9 (MMP9). In vivo validation supported these findings, as FKA administration showed protective effects on kidney function and histology with the downregulation of extracellular matrix (ECM) markers, such as fibronectin (FN) and transforming growth factor β1 (TGF-β1), along with reduced expression of NF-κB1 and MMP9. These findings indicate that FKA could be a valuable therapeutic candidate for managing CKD by targeting NF-κB1 and MMP9.\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"1015-1028"},"PeriodicalIF":3.3,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149457","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

USP39 Depletion Plays Repressive Roles in Laryngeal Squamous Cell Carcinoma Development USP39缺失在喉部鳞状细胞癌发展中起抑制作用

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-22 DOI: 10.1002/cbin.70035

Wen Xie, Lei Zhang, Xiaoyan Hu, Yahua Zhong, Zheng Li

{"title":"USP39 Depletion Plays Repressive Roles in Laryngeal Squamous Cell Carcinoma Development","authors":"Wen Xie, Lei Zhang, Xiaoyan Hu, Yahua Zhong, Zheng Li","doi":"10.1002/cbin.70035","DOIUrl":"10.1002/cbin.70035","url":null,"abstract":"<div>\u0000 \u0000 Laryngeal squamous cell carcinoma (LSCC) is a prevalent malignant tumor of the upper respiratory tract. Ubiquitin-specific protease 39 (USP39) has been identified as an oncogenic regulator in various malignant tumors; however, its specific roles in LSCC remain unexplored. In this study, immunohistochemistry was employed to assess USP39 expression in LSCC tissues and adjacent normal tissues. Subsequently, a USP39 knockdown cellular model was established to investigate its effects on cell proliferation, apoptosis, and migration through Celigo cell counting, colony formation, flow cytometry, and transwell assays, respectively. A tumor-bearing animal model was established to verify the impact of USP39 on LSCC In Vivo. Co-immunoprecipitation (Co-IP) assay was used to validate protein–protein interaction. Our results suggested that USP39 was highly expressed in laryngeal cancer tissues, which exhibited a correlation with lymphatic metastasis. In Vitro loss-of-function experiments revealed that depletion of USP39 suppressed cell proliferation and migration, and induced apoptosis in LSCC cells. Furthermore, silencing USP39 restrained tumor growth silencing USP39 In Vivo. Mechanistically, USP39 was found to interact with and upregulated Aurora kinase B (AURKB). AURKB depletion attenuated the protumorigenic effects of USP39 overexpression. Additionally, USP39 enhanced ERK1/2 phosphorylation, and pharmacological inhibition of ERK1/2 abrogated USP39-driven proliferative and clonogenic capacities. In summary, this study underscores the significance of USP39 in the development of LSCC, positioning it as a promising therapeutic target for LSCC treatment.</div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"1003-1014"},"PeriodicalIF":3.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126269","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

Cyclophosphamide Induces Glioblastoma Tumor Cell Death and Oxidative Stress Through the Increase of TRPM2 Channel Stimulation: The Role of Carvacrol. 环磷酰胺通过增加TRPM2通道刺激诱导胶质母细胞瘤细胞死亡和氧化应激：香芹酚的作用。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-05-22 DOI: 10.1002/cbin.70039

Kemal Ertilav, Mustafa Nazıroğlu

{"title":"Cyclophosphamide Induces Glioblastoma Tumor Cell Death and Oxidative Stress Through the Increase of TRPM2 Channel Stimulation: The Role of Carvacrol.","authors":"Kemal Ertilav, Mustafa Nazıroğlu","doi":"10.1002/cbin.70039","DOIUrl":"https://doi.org/10.1002/cbin.70039","url":null,"abstract":"Cyclophosphamide (CP) damages glioblastoma cells by producing an excessive amount of intracellular (iROS) and mitochondrial (mROS) reactive oxygen species. Both iROS and mROS are produced when TRPM2 is activated, but they are decreased when carvacrol (CAR) and N-(p-amylcinnamoyl) anthranilic acid (ACA) inhibit it. Therefore, iROS, and mROS via upregulating Ca2+ influx and apoptosis in glioblastoma (DBTRG-05MG) cells, CP-mediated TRPM2 stimulation may cause oxidant and apoptotic activities. We investigated how TRPM2 activation not only promotes DBTRG-05MG death but also modifies oxidative damage and apoptosis to counteract the effects of ACA and CAR. The groups of control (CN), CAR (200 μM for 24 h), CP (2 mM for 24 h), and CP + CAR were induced in the DBTRG-05MG. While cytosolic free Ca2+ levels decreased in the cells as a result of the CAR and ACA treatments, they were further elevated in the CP group by the stimulation of TRPM2 (H2O2). The cells in the CP group had higher levels of dead cell percentage, apoptosis, mitochondrial membrane dysfunction, mROS, iROS, and caspases -3, -8, and -9 than the CN and CAR cells, although their levels were lower in the CP + CAR than in the CP only. CAR incubation increased the CP-induced glutathione concentration and cell viability percentage declines. In summary, the anticancer effect of CP was enhanced by TRPM2 stimulation, while CP-induced oxidative stress and DBTRG-05MG death were reduced by TRPM2 suppression when CAR was treated. TRPM2 activation may be a possible tumor killer channel due to oxidative glioma damage caused by CP.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118959","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