Cell Biochemistry and Biophysics最新文献

{"title":"Correction: Icariside II Alleviates Chondrocyte Inflammatory Injury by Inhibiting the TNIP2/NF-κB Pathway.","authors":"Jiajun Mei, Hongkui Ke, Junsong Zhu","doi":"10.1007/s12013-025-01769-4","DOIUrl":"10.1007/s12013-025-01769-4","url":null,"abstract":"","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3995-3997"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Chaperone-Mediated Autophagy Reactivation Protects Against Severe Acute Pancreatitis-Associated Liver Injury Through Upregulating Keap1/Nrf2 Signaling Pathway and Inhibiting NLRP3 Inflammasome Activation.","authors":"Zhongbiao Li, Yue Yu, Xihao Zhao, Yue Qu, Jiang Wang, Dianliang Zhang","doi":"10.1007/s12013-025-01760-z","DOIUrl":"10.1007/s12013-025-01760-z","url":null,"abstract":"","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3991"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin Inhibits the Development of Helicobacter pylori-Associated Gastritis by Regulating the ERK-MMP10-IL-1β Axis.","authors":"Wenying Zhu, Qiuxia Li, Min Kang","doi":"10.1007/s12013-025-01739-w","DOIUrl":"10.1007/s12013-025-01739-w","url":null,"abstract":"<p><p>Helicobacter pylori infection is one of the most common factors inducing gastric mucosal inflammation. Upon infecting gastric epithelial cells, H. pylori generates reactive oxygen species (ROS), which act as inducers of matrix metalloproteinases (MMPs). ROS can regulate MMP gene expression and promote their production through the ERK signaling pathway, with MMP-10 being a primary MMP induced during H. pylori infection. By mediating the remodeling of the gastric epithelial and lamina propria layers, MMP-10 enhances H. pylori colonization and its pro-inflammatory effects. As resistance to eradication therapies has significantly increased, H. pylori eradication rates have continued to decline. We investigated the antioxidant effects of metformin on cell viability, migration, and invasion. The in vitro levels of ROS, MMP-10, and the inflammatory factor IL-1β in H. pylori-infected gastric epithelial cells were assessed to determine whether metformin could alleviate H. pylori-induced inflammation and elucidate its potential mechanisms of action. These findings may provide novel insights into adjunctive therapeutic strategies for the effective clinical eradication of H. pylori infection. The results indicated that H. pylori infection significantly increased ROS production, activating the ERK pathway and upregulating MMP-10 expression, which enhanced cellular invasion and the inflammatory response. Metformin intervention effectively blocked this pathological cascade, significantly reducing ROS levels, MMP-10 expression, and the release of inflammatory cytokines, exerting an inhibitory effect on H. pylori-induced inflammation and demonstrating the potential application of metformin as a therapeutic agent.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3597-3606"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143778656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-218 Exhibits Anti-Leukemia Effects by Targeting CTNND2 in Primary Acute Erythroid Leukemia HEL Cells.","authors":"Ming-Qiang Chu, Ting-Juan Zhang, Zi-Qi Liu, Qian Yang, Ting-Ting Du, Min-Jie Zhang, Ye Jin, Yong-Jie Cao, Xiang-Mei Wen, Zi-Jun Xu, Yang-Jing Zhao, Jiang Lin, Jun Qian, Jing-Dong Zhou","doi":"10.1007/s12013-025-01722-5","DOIUrl":"10.1007/s12013-025-01722-5","url":null,"abstract":"<p><p>Acute erythroid leukemia (AEL) is a rare acute myeloid leukemia (AML) subtype that is highly aggressive and is associated with a poor prognosis. Notably, the blockage of erythroid differentiation represents a significant factor in the pathogenesis of erythroleukemia. Prior studies indicated that miR-218 inhibited the erythroid differentiation in a chronic myeloid leukemia (CML)-derived erythroleukemia cell line K562. However, functions of miR-218 in primary AEL remains to be elucidated. To address this gap, functions of miR-218 in HEL cells were evaluated through cell differentiation, cell proliferation, colony formation, cell cycle and cell apoptosis experiments. Subsequently, the targeted downstream genes of miR-218 were identified by the transcriptome sequencing and bioinformatic research, of which demonstrated by the dual-luciferase reporter experiment. Finally, the underlying mechanism of miR-218 in leukemogenesis was identified by enrichment analysis and was validated by western blot (WB) assays. Intriguingly, enhanced miR-218 showed no effect on the erythroid differentiation in HEL cells by determination of the expression of erythroid markers including GATA1, KLF1, TFRC and GYPA. However, miR-218 overexpression in HEL cells presented a markedly anti-proliferative and pro-apoptotic effects, inhibited colony formation and G0/G1 arrest. Transcriptome sequencing and bioinformatics analysis revealed that CTNND2 as the candidate gene of miR-218 within its 3'-untranslated region (3'-UTR) could be bonded by it. Reduced expression level of CTNND2 was further demonstrated by quantitative-PCR and WB after miR-218 overexpression in HEL cells. Furthermore, the luciferase report assay revealed that the CTNND2 production was reduced with its 3'-UTR region was bonded by miR-218. In addition, MAPK signaling pathway was identified and validated as the potential functional pathway involved in leukemogenesis caused by miR-218 overexpression in HEL cells. In summary, miR-218 exhibits anti-proliferative and pro-apoptotic functions by targeting CTNND2 and modulating MAPK signaling in HEL cells, yet it has no impact on the erythroid differentiation process.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3395-3405"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143655620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isogarcinol Reduces MARS Levels and Deactivates the PI3K/AKT Pathway to Suppress the Malignant Properties of Breast Cancer Cells.","authors":"Dechao Zhang, Yunhai Chu, Meng Li, Lin Du","doi":"10.1007/s12013-025-01727-0","DOIUrl":"10.1007/s12013-025-01727-0","url":null,"abstract":"<p><p>Natural products and their extracts are increasingly considered valuable sources for small-molecule anti-cancer drugs. This study investigates the biological impacts of isogarcinol (ISO) on breast cancer (BC) cells and delves into the underlying mechanisms. In vitro, treatment of ISO at 13 μM substantially reduced the viability, proliferation, and mobility of BC. In vivo, ISO treatment at 5, 10, and 15 mg/kg reduced the tumorigenic activity of MDA-MB-231 cells and decreased the levels of Ki-67 and CD31. ISO exerted tumor suppressive effects by reducing the protein level of methionyl-tRNA synthetase (MARS), as the MARS restoration reversed the trends induced by ISO. Phosphorylation levels of phosphatidyl inositol 3 (PI3K) and protein kinase B (AKT) in BC cells were reduced by ISO but restored by MARS. In the presence of MARS upregulation, further treatment of Alpelisib, a suppressor of the PI3K/AKT pathway, suppressed the malignant properties of BC cells. Collectively, these results demonstrate that ISO curbs the malignant behavior of BC cells by reducing the MARS protein level and deactivating the PI3K/AKT pathway. ISO may be considered a promising regimen for the management of BC.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3437-3449"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143690730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Paeonol of Total Glucosides of White Peony Regulates the Differentiation of CD4+Treg Cells through the EP300/Foxp3 Axis to Relieve Pulmonary Fibrosis in Mice.","authors":"Muyun Yan, Qing Wang, Hongzhong Yang, Da Liu, Weijun Liang, Huamei Chen","doi":"10.1007/s12013-025-01770-x","DOIUrl":"10.1007/s12013-025-01770-x","url":null,"abstract":"<p><p>Pulmonary fibrosis is a chronic progressive lung disease that can lead to lung structural damage and respiratory failure. This study aimed to investigate whether paeonol could improve pulmonary fibrosis in mice by regulating through the EP300/Foxp3 axis. We established a mouse model of pulmonary fibrosis. Total glucosides of white peony (TGP) were used to treat the animal model, and lung injury was observed using HE and Masson staining. Inflammatory factor levels in bronchoalveolar lavage fluid were detected using ELISA. Network pharmacology analysis was conducted to explore the components, shared targets, and signaling pathways of pulmonary fibrosis and TGP. Molecular docking was performed to observe the binding of paeonol, a component of TGP, to the target EP300. CD4+T cells were collected and co-cultured with MPPF cells, followed by intervention with TGP and paeonol. The ratio of CD4+T/Treg cells was measured in vitro, and immunofluorescence was used to detect the intensity of α-SMA. Network pharmacology revealed that one of the key components of TGP is paeonol, and the signaling pathway associated with pulmonary fibrosis is the Foxp3 signaling pathway. TGP effectively inhibited the secretion of lung inflammatory factors TGF-β1, IFN-γ, IL-2, and IL-17 in mic. Paeonol, an effective component of TGP, could bind to EP300 at the molecular level. Both TGP and paeonol inhibited the expression of EP300 in CD4+T and MPPF cells, enhanced the proportion of Treg cells in CD4+T, and reduced the expression of Collagen I and α-SMA in MPPF cells. TGP can effectively inhibit lung inflammation and fibrosis progression in mice. Paeonol regulating CD4+Treg cell differentiation through the EP300/Foxp3 axis. This study may provide new insights into how TGP improves pulmonary fibrosis in mice.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3959-3970"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphorylation Enhanced the anti-cancer Therapeutic Activity of Larix sibirica-derived Arabinogalactan in Hepatocellular Carcinoma.","authors":"Maya P Shetty, Prasad Tambe, Komal Rana, Suresh D Kulkarni, Pradip Chaudhari, Sanjay Bharati","doi":"10.1007/s12013-025-01876-2","DOIUrl":"https://doi.org/10.1007/s12013-025-01876-2","url":null,"abstract":"","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144938224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PMEPA1 Binds NEDD4L to Inhibit the Malignant Progression of Multiple Myeloma by Inactivating Wnt/β-Catenin Signaling.","authors":"Shanshan Hu, Xinfang Gao, Yan Zhu, Fangjing Shi, Li Huang","doi":"10.1007/s12013-025-01674-w","DOIUrl":"10.1007/s12013-025-01674-w","url":null,"abstract":"<p><p>Multiple myeloma (MM) is an incurable hematological malignancy with increasing prevalence. Prostate transmembrane androgen inducible protein 1 (PMEPA1) is positively associated with overall survival in MM patients, but the exact functions and mechanisms of PMEPA1 in MM have yet to be elucidated. PMEPA1 and neural precursor cell-expressed developmentally downregulated gene 4L (NEDD4L) levels in MM cells were examined. In RPMI-8226 cells with PMEPA1 overexpression or/and NEDD4L knockdown, cell proliferation, cycle distribution and apoptosis were evaluated with the application of CCK-8, EDU staining and flow cytometry. The BioGrid website and HDOCK SERVER were applied for predicting the binding between PMEPA1 and NEDD4L, which was checked by co-immunoprecipitation. Besides, the levels of proteins associated with proliferation (Ki67 and PCNA), apoptosis (Bcl-2, Bax and cleaved caspase3) and Wnt/β-catenin signaling (β-catenin, c-Myc and cyclin D1) was detected with immunoblotting. Finally, LiCl, an activator of Wnt/β-catenin pathway, was employed to treat RPMI-8226 cells to analyze the proliferation, cycle distribution and apoptosis of MM cells. As a result, PMEPA1 and NEDD4L were expressed at low levels in MM cells. PMEPA1 upregulation repressed proliferation induced cycle arrest and facilitated apoptosis of MM cells. Moreover, PMEPA1 bound to NEDD4L and upregulated NEDD4L expression in RPMI-8226 cells. Functionally, NEDD4L knockdown attenuated the influences of PMEPA1 overexpression on the proliferation, cycle distribution and apoptosis of RPMI-8226 cells. Additionally, PMEPA1 notably downregulated β-catenin, c-Myc and cyclin D1 expression in RPMI-8226 cells, which was abrogated by NEDD4L silencing. Further adding LiCl in RPMI-8226 cells led to the enhanced malignant biological behaviors. Collectively, PMEPA1 damaged MM progression through binding NEDD4L to inactivate Wnt/β-catenin signaling, which may be helpful to develop promising targets for MM treatment.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3971-3981"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergistic Enhancement of Apo2L/TRAIL and DR4-Induced Apoptosis by Arsenic Trioxide in Triple-Negative Breast Cancer Cells: A Comparison to Conventional Chemotherapy.","authors":"Soraya Moomivand, Mohsen Nikbakht, Ahmad Majd, Maryam Bikhof Torbati, Seyed Asadoullah Mousavi","doi":"10.1007/s12013-025-01764-9","DOIUrl":"10.1007/s12013-025-01764-9","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype lacking hormonal and HER2 receptors, making it highly resistant to treatment. Apo2L/TRAIL, a tumor necrosis factor-related ligand, induces apoptosis in cancer cells via the death receptor DR4. However, TNBC often develops resistance to TRAIL-mediated apoptosis, limiting its therapeutic potential. This study investigates whether arsenic trioxide (ATO) can overcome TRAIL resistance by modulating the Apo2L/TRAIL pathway and enhancing the effects of carboplatin (CP) and cyclophosphamide (CY). TNBC cell lines BT-20 and MDA-MB-231 were treated with ATO, CP, CY, and their combinations. Cell viability was measured using the MTT assay, while real-time PCR and Western blot analysis assessed Apo2L/TRAIL and DR4 expression. Statistical analysis was performed using ANOVA with Dunnett's post hoc test. ATO induced dose-dependent cytotoxicity in TNBC cells, which was significantly enhanced in combination treatments. The highest reductions in cell viability were observed with 3 µM ATO plus 5000 µM CP or 500 µM CY (p < 0.0001). ATO markedly upregulated Apo2L/TRAIL and DR4 at both mRNA and protein levels, with the most pronounced effects seen in ATO-CY combinations. These findings indicate that ATO sensitizes TNBC cells to TRAIL-mediated apoptosis by upregulating DR4 and Apo2L/TRAIL, while also exhibiting strong synergistic cytotoxicity with CP and CY. This highlights ATO's potential as an adjuvant therapy to improve TNBC treatment efficacy and overcome chemoresistance, warranting further clinical exploration.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3905-3917"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NanoBiT-based Analysis of Canine SOD1 Protein Dynamics: Understanding the Role of CCS and Ebselen Derivatives as Potential Therapeutics for Canine Degenerative Myelopathy.","authors":"Sakura Hirose, Yui Kobatake, Norihiro Tada, Mahmoud Kandeel, Akichika Itoh, Kentaro Oh-Hashi","doi":"10.1007/s12013-025-01768-5","DOIUrl":"10.1007/s12013-025-01768-5","url":null,"abstract":"<p><p>Canine degenerative myelopathy (DM) is a progressive neurodegenerative disorder that shares common pathological features with amyotrophic lateral sclerosis (ALS) in humans. Both diseases are linked to mutations in the superoxide dismutase 1 (SOD1) gene. Understanding the molecular differences between wild-type (WT) and mutant SOD1 proteins is critical for developing therapeutic strategies. In this study, we employed the NanoLuc complementation (NanoBiT) reporter system to investigate the expression and functional differences between WT and E40K mutant canine SOD1 to assess the therapeutic potential of copper chaperone for SOD1 (CCS) and ebselen derivatives. E40K cSOD1 displayed significantly reduced luciferase activity compared to WT cSOD1 in all NanoBiT-tagged combinations, indicating altered homodimerization and protein stability. Co-transfection with CCS increased both WT and mutant cSOD1 protein levels and reporter activities, with a more pronounced effect on the E40K mutant. Ebselen treatment enhanced luciferase activity, particularly in E40K cSOD1-expressing cells. Two compounds (compounds 2 and 5) were stronger than the parent compound in improving mutant cSOD1-derived NanoBiT activities. Additionally, molecular docking simulations revealed stronger binding affinities of ebselen and its derivatives to E40K cSOD1, suggesting potential therapeutic benefits. In conclusion, the NanoLuc reporter system offers a valuable tool for screening potential therapeutics for SOD1-linked neurodegenerative diseases. CCS and ebselen derivatives exhibited promising effects on SOD1 activity, providing a basis for future therapeutic strategies targeting both DM and ALS.</p>","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"3945-3958"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}