Biochemical and biophysical research communications最新文献_第2页

Tetrahydroquinoline/4,5-dihydroisoxazoline hybrids counteracts multidrug resistance by inhibiting MRP1-mediated drug efflux 四氢喹啉/4,5-二氢异恶唑啉杂合体通过抑制mrp1介导的药物外排来抵消多药耐药

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-23 DOI: 10.1016/j.bbrc.2025.152074

Giovana da Silva Pereira , Luis C. Vesga , Gustavo Scheiffer , Ingrid Fatima Zattoni , Bruna Estelita Ruginsk , Cristian C. Bernal , Arnold R. Romero Bohórquez , Stelia Carolina Mendez-Sanchez , Azam Rashidian , Antti Poso , Fabiane Gomes de Moraes Rego , Geraldo Picheth , Vivian Rotuno Moure , Thales Kronenberger , Glaucio Valdameri

{"title":"Tetrahydroquinoline/4,5-dihydroisoxazoline hybrids counteracts multidrug resistance by inhibiting MRP1-mediated drug efflux","authors":"Giovana da Silva Pereira , Luis C. Vesga , Gustavo Scheiffer , Ingrid Fatima Zattoni , Bruna Estelita Ruginsk , Cristian C. Bernal , Arnold R. Romero Bohórquez , Stelia Carolina Mendez-Sanchez , Azam Rashidian , Antti Poso , Fabiane Gomes de Moraes Rego , Geraldo Picheth , Vivian Rotuno Moure , Thales Kronenberger , Glaucio Valdameri","doi":"10.1016/j.bbrc.2025.152074","DOIUrl":"10.1016/j.bbrc.2025.152074","url":null,"abstract":"<div><div>Current cancer treatments are challenged by multidrug resistance (MDR). MDR can be a result of overexpression of ABC transporters, such as the multidrug resistance-associated protein 1 (MRP1). They act as efflux pumps expelling chemotherapy outside of the cells, and ABC transport inhibitors can overcome MDR. To identify and characterize new MRP1 inhibitors, 16 tetrahydroquinoline/4,5-dihydroisoxazole derivatives (<strong>A1</strong> - <strong>D4</strong>) were tested in stably transfected cells overexpressing MRP1 (BHK21-MRP1). Compounds <strong>A1</strong> and <strong>D1</strong> showed the best results (IC<sub>50</sub> of 0.58 and 2.74 μM, respectively). They showed low cytotoxicity and were not transported by MRP1. Compound <strong>A1</strong> showed a therapeutic ratio (TR) higher than 170. Our structural model's analysis suggests that <strong>A1</strong> fluctuates between the P and H-pockets in the MRP1. <strong>A1</strong> interacts with Gln377 and Lys332 and is further supported by π-contacts with Trp1246 and Phe594. The different binding site of <strong>A1</strong> and the substrate calcein-AM, as revealed by the molecular modelling analysis, was confirmed by the non-competitive inhibition observed by flow cytometry. The major significance lies in the confirmation of the <strong>A1</strong> and <strong>D1</strong> inhibition, as they improved the effect of chemotherapeutics (etoposide and daunorubicin) in cells overexpressing MRP1. Together, these results demonstrated the potential of <strong>A1</strong> to follow in pre-clinical studies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"774 ","pages":"Article 152074"},"PeriodicalIF":2.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170739","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

Metabolic reprogramming on breast cancer stem Cells: Proliferation and self-renewal, epithelial-mesenchymal transition (EMT), and drug resistance 乳腺癌干细胞的代谢重编程：增殖和自我更新，上皮-间质转化（EMT）和耐药性

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-23 DOI: 10.1016/j.bbrc.2025.152079

Fuxin Chen , Bingjie Zhao , Yuxuan Tian , Qiang Liu , Bin Zhang

{"title":"Metabolic reprogramming on breast cancer stem Cells: Proliferation and self-renewal, epithelial-mesenchymal transition (EMT), and drug resistance","authors":"Fuxin Chen , Bingjie Zhao , Yuxuan Tian , Qiang Liu , Bin Zhang","doi":"10.1016/j.bbrc.2025.152079","DOIUrl":"10.1016/j.bbrc.2025.152079","url":null,"abstract":"<div><div>Tumors are complex diseases caused by the proliferation and metastasis of malignant cells, posing a significant threat to human health due to their high incidence and mortality rates. Breast cancer currently has the highest incidence among cancers worldwide, and breast cancer stem cells (BCSCs) play a crucial role in the onset, malignant progression, and poor prognosis of breast cancer. With advancing research, metabolic reprogramming of tumor cells has been identified as a key factor in tumor development, metastasis, and drug resistance. Therefore, this review explores the targeting of metabolic reprogramming in BCSCs, examining the regulation of glycolysis, oxidative phosphorylation (OXPHOS), lipid metabolism, and amino acid metabolism within BCSCs, and their impact on proliferation, self-renewal, epithelial-mesenchymal transition (EMT), and acquired drug resistance. Additionally, the review discusses the potential of metabolism-related drugs in the prevention and treatment of breast cancer. In summary, this review provides new strategies for the clinical management of breast cancer.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"774 ","pages":"Article 152079"},"PeriodicalIF":2.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144170273","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

Screening ligands interacting with NDUFS3 from Oroxylum indicum extract using bioaffinity ultrafiltration combined with in vitro protein purification 采用生物亲和超滤结合体外蛋白纯化技术筛选籼米提取物中与NDUFS3相互作用的配体

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-23 DOI: 10.1016/j.bbrc.2025.152078

Ya-fei Ma , Xiao-xue Zhang , De-zhi Kong , De-qiang Li

{"title":"Screening ligands interacting with NDUFS3 from Oroxylum indicum extract using bioaffinity ultrafiltration combined with in vitro protein purification","authors":"Ya-fei Ma , Xiao-xue Zhang , De-zhi Kong , De-qiang Li","doi":"10.1016/j.bbrc.2025.152078","DOIUrl":"10.1016/j.bbrc.2025.152078","url":null,"abstract":"<div><div><em>Oroxylum indicum</em> (<em>O. indicum</em>) is a common traditional Chinese medicine, but its neuroprotective effects in Parkinson's disease (PD) model have not been fully elaborated. Mitochondrial complex I dysfunction is the core pathology of oxidative stress injury in PD, and the mechanism of regulating the activity of its key subunit NADH: Ubiquinone Oxidoreductase Core Subunit S3 (NDUFS3) has not been clarified. To explore the potential therapeutic effects of <em>O</em>. <em>indicum</em> on PD and reveal the potential active compounds and molecular mechanism of action behind the treatment of PD by <em>O indicum</em> extract (OIE), in the present study, the mitochondrial complex I subunit NDUFS3 was selected as the PD disease target, and a “three-in-one” system combing target purification of NDUFS3 protein, affinity ultrafiltration screening and validation-analysis of molecular mechanism was constructed. Results suggest that the active compounds in <em>O indicum</em> screened by affinity screening can target and regulate the expression of NDUFS3, lower the mitochondrial membrane potential, reduce oxidative stress, and increase the ATP content, thus exerting anti-PD effects at the cellular and animal levels. The integrated approach of protein purification, affinity ultrafiltration screening and pharmacological validation is pivotal for efficiently identifying active compounds and uncovering their mechanisms in anti-PD research, thereby proving a reference for drug discovery of neurodegenerative diseases.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"773 ","pages":"Article 152078"},"PeriodicalIF":2.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138405","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

Crystal structure and inhibition mechanism of AcrIIA11 AcrIIA11的晶体结构及抑制机理

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-22 DOI: 10.1016/j.bbrc.2025.152073

Xueli Cao , Zirui Gao , Peipei Yin , Hao Wang , Lingguang Yang

{"title":"Crystal structure and inhibition mechanism of AcrIIA11","authors":"Xueli Cao , Zirui Gao , Peipei Yin , Hao Wang , Lingguang Yang","doi":"10.1016/j.bbrc.2025.152073","DOIUrl":"10.1016/j.bbrc.2025.152073","url":null,"abstract":"<div><div>Anti-CRISPR (Acr) proteins are naturally evolved inhibitors that precisely target and suppress CRISPR-Cas systems, representing a sophisticated molecular arms race between bacteriophages and their bacterial hosts. While Class 1 systems dominate among sequenced prokaryotic genomes, Class 2 systems remain primary sources of editing tools. Here, we report the structural and mechanistic characterization of AcrIIA11, an anti-CRISPR protein that simultaneously inhibits <em>Streptococcus pyogenes</em> (SpyCas9) and <em>Staphylococcus aureus</em> Cas9 (SauCas9). The 3.2 Å crystal structure reveals a compact α/β fold with distinct electropositive clefts implicated in DNA binding. While DALI analysis identified structural homology to transcriptional regulators and the RecA inhibitor PsiB (RMSD 3.3 Å), functional studies established that AcrIIA11 forms stable ternary complexes with both Cas9 orthologs and sgRNA. Biochemical assays demonstrated stronger inhibition of SauCas9 compared to SpyCas9, with EMSA revealing a critical dichotomy: AcrIIA11 maintains SauCas9-sgRNA binding to specific target DNA while completely blocking cleavage activity. Computational docking localizes AcrIIA11 at the HNH-RuvC interface without obstructing DNA-binding channels in SauCas9, suggesting allosteric inhibition through HNH domain displacement. This work establishes AcrIIA11 as a dual-purpose Cas9 inhibitor that preserves target recognition while inactivating nuclease function—a mechanism with potential applications in precision CRISPR control.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"772 ","pages":"Article 152073"},"PeriodicalIF":2.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131402","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

Pexidartinib impairs liver mitochondrial functions causing cell death in primary human hepatocytes at clinically relevant concentrations 培西达替尼在临床相关浓度下损害肝脏线粒体功能，导致原代人肝细胞死亡

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-22 DOI: 10.1016/j.bbrc.2025.152075

Qiang Shi , Lijun Ren , Katy Papineau , Xi Yang , Li Pang , Jessica Hawes Oliphant , Laura Schnackenberg , William Mattes

{"title":"Pexidartinib impairs liver mitochondrial functions causing cell death in primary human hepatocytes at clinically relevant concentrations","authors":"Qiang Shi , Lijun Ren , Katy Papineau , Xi Yang , Li Pang , Jessica Hawes Oliphant , Laura Schnackenberg , William Mattes","doi":"10.1016/j.bbrc.2025.152075","DOIUrl":"10.1016/j.bbrc.2025.152075","url":null,"abstract":"<div><div>Pexidartinib is a regulatory agency approved small molecule kinase inhibitor (KI) with a boxed warning for hepatotoxicity, and FDA requires a Risk Evaluation and Mitigation Strategy (REMS) to mitigate such risk. The mechanism of pexidartinib hepatotoxicity is poorly understood. As mitochondrial injury and hepatocyte toxicity have been proposed to be a shared mechanism for the hepatotoxicity induced by many KIs, here we examined pexidartinib for such liabilities. Freshly isolated rat liver mitochondria, submitochondrial fractions, and cryopreserved primary human hepatocytes (PHHs) – the gold standard in vitro model for drug hepatotoxicity – were treated with pexidartinib at clinically relevant concentrations, and mitochondrial functions and cytotoxicity were assessed. In isolated mitochondria, the state 3 oxygen consumption rates of glutamate/malate- and succinate-driven respiration were both decreased by pexidartinib, while the state 4 oxygen consumption rates were unaffected. In submitochondrial fractions, the activities of respiratory chain complex (RCC) I and V, but not II, III, IV, were significantly inhibited by pexidartinib. In PHHs, as measured by a Seahorse system, pexidartinib decreased basal, spare, maximal, and adenosine triphosphate (ATP)-linked respirations at 2 h in the absence of cell death. Pexidartinib also inhibited cellular ATP level, increased reactive oxygen species, and caused cell death after 24 h. However, activities of caspases were unaffected. Importantly, the detrimental effects noted above occurred at pexidartinib concentrations of 0.5- to 2.5-fold of the human peak blood concentration (C<sub>max</sub>) achieved with the recommended therapeutic dose. These data suggest that mitochondrial injury and hepatocyte toxicity are involved in the mechanism of pexidartinib-induced hepatotoxicity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"773 ","pages":"Article 152075"},"PeriodicalIF":2.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144134711","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

Differential expression of lysine-acetylated proteins in the anti-inflammatory effects of luteolin-gadolinium on macrophages 木犀草素钆对巨噬细胞抗炎作用中赖氨酸乙酰化蛋白的差异表达

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-22 DOI: 10.1016/j.bbrc.2025.152072

Hongjia Zhang , Huhu Tian , Yanqin Yu , Jinqi Hao , Liquan Wang , Ruize Qiu , Xiuchun Wang , Xiaoyu Wang , Hongzhang Cao , Jihai Shi

{"title":"Differential expression of lysine-acetylated proteins in the anti-inflammatory effects of luteolin-gadolinium on macrophages","authors":"Hongjia Zhang , Huhu Tian , Yanqin Yu , Jinqi Hao , Liquan Wang , Ruize Qiu , Xiuchun Wang , Xiaoyu Wang , Hongzhang Cao , Jihai Shi","doi":"10.1016/j.bbrc.2025.152072","DOIUrl":"10.1016/j.bbrc.2025.152072","url":null,"abstract":"<div><div>This study investigates the anti-inflammatory mechanisms of luteolin-gadolinium rare earth complexes (LutGdRCS) in LPS-activated macrophages, focusing on lysine-acetylated protein regulation. Transcriptional (qPCR), proteomic (4D-DIA tandem mass spectrometry), and functional analyses revealed that LutGdRCS significantly downregulated pro-inflammatory mediators (iNOS, IL-6, IL-1β) and nitric oxide (NO) levels. Quantitative acetylome profiling identified 1260 lysine-acetylation sites across 796 proteins, with 775 upregulated and 485 downregulated sites. Key proteins—Eef2, Rpl5, and Atp5c1—emerged as central hubs in protein-protein interaction networks, while Atp5f1cK_89 was identified as a critical deacetylation site linked to mitochondrial ATP synthase activity. Subcellular localization analysis showed cytoplasmic (34.7 %), nuclear (34.1 %), and mitochondrial (10.6 %) enrichment of modified proteins. Pathway mapping highlighted LutGdRCS-driven modulation of NF-κB, JAK-STAT, oxidative phosphorylation, and nitrogen metabolism pathways. Bioinformatic clustering further revealed altered ubiquitin ligase activity, antioxidant responses, and ribosomal functions. These findings demonstrate that LutGdRCS attenuates inflammation by dynamically regulating lysine acetylation, particularly through mitochondrial energy metabolism and immune signaling pathways. The study positions LutGdRCS as a novel rare earth-based therapeutic candidate for inflammatory disorders, offering mechanistic insights into its acetylome-level anti-inflammatory effects.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"773 ","pages":"Article 152072"},"PeriodicalIF":2.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144138402","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

IRF2-driven upregulation of OAS3 promotes AML cell proliferation by modulating the JAK-STAT signaling pathway irf2驱动的OAS3上调通过调节JAK-STAT信号通路促进AML细胞增殖

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-21 DOI: 10.1016/j.bbrc.2025.152064

Xi Zhang , Liang Zhong , Li Zhai , Haitao Li , Beizhong Liu

{"title":"IRF2-driven upregulation of OAS3 promotes AML cell proliferation by modulating the JAK-STAT signaling pathway","authors":"Xi Zhang , Liang Zhong , Li Zhai , Haitao Li , Beizhong Liu","doi":"10.1016/j.bbrc.2025.152064","DOIUrl":"10.1016/j.bbrc.2025.152064","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) presents significant treatment challenges due to its heterogeneity and resistance to conventional therapies. This study explored the role of 2′-5′-oligoadenylate synthetase 3 (OAS3) in AML progression and its potential as a prognostic and therapeutic biomarker. Through bioinformatics analysis, OAS3 was found to be significantly upregulated in AML patients and associated with poor clinical outcomes. Functional assays in AML cell lines revealed that silencing OAS3 suppressed cell proliferation, induced G1 phase arrest, and promoted apoptosis, while its overexpression enhanced cell growth. Pathway analysis and western blotting demonstrated that OAS3 regulates the JAK-STAT signaling pathway. Further investigation revealed that interferon regulatory factor 2 (IRF2) acts as a transcription factor that binds to the promoter region of OAS3 and enhances its expression, thereby indirectly modulating the JAK-STAT pathway. Cotransfection experiments with IRF2 and si-OAS3 supported this regulatory mechanism. In vivo studies using a xenograft model and subsequent immunohistochemical analysis of tumor specimens confirmed the role of OAS3 in AML progression. These findings highlight OAS3 as a critical player in AML pathogenesis, functioning through the JAK-STAT pathway activation under the transcriptional control of IRF2. The study suggests that OAS3 could serve as a valuable prognostic marker and therapeutic target, offering a promising avenue to improve AML treatment outcomes.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"772 ","pages":"Article 152064"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130912","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 role of Sine Oculis Homeobox Homolog 2 in colon Cancer: Insights into prognosis, immune regulation, and therapeutic implications Sine Oculis Homeobox同源物2在结肠癌中的作用：对预后、免疫调节和治疗意义的见解

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-21 DOI: 10.1016/j.bbrc.2025.152038

Shicheng Zhou , Dan Jiang , Yu Liu , Qin Wang , Manyi Hu , Kangfu Dai , Lin Chen , Tianming Zhang , Cheng Cai , Jianping Wang

{"title":"The role of Sine Oculis Homeobox Homolog 2 in colon Cancer: Insights into prognosis, immune regulation, and therapeutic implications","authors":"Shicheng Zhou , Dan Jiang , Yu Liu , Qin Wang , Manyi Hu , Kangfu Dai , Lin Chen , Tianming Zhang , Cheng Cai , Jianping Wang","doi":"10.1016/j.bbrc.2025.152038","DOIUrl":"10.1016/j.bbrc.2025.152038","url":null,"abstract":"<div><div>Colon cancer (CC) remains a significant global health burden, and the search for novel prognostic biomarkers and therapeutic targets is crucial. This study comprehensively analyzed the role of SIX2 (Sine Oculis Homeobox Homolog 2) in CC. Utilizing data from TCGA, GTEx, and CCLE databases, differential expression of SIX2 was observed in multiple cancers, with significant upregulation in many tumors compared to normal tissues. In CC, SIX2's differential expression was notable. Cox regression analysis revealed its prognostic significance, with overexpression associated with poor survival outcomes. SIX2 was strongly associated with gene alterations and correlated with key signaling pathways like WNT and TGF-β. In the tumor microenvironment, SIX2 was related to immune cell infiltration and immune-related molecules. Notably, in CC, it was associated with immunosuppressive cells and checkpoint molecules. Additionally, ABT737 was found to sensitize tumor immunotherapy in the context of SIX2. Animal experiments demonstrated that ABT737 effectively restricted the growth of CC in mice, and its combination with antiPD-1 immunotherapy was more effective. It could reduce the infiltration of CD163+ tumor-associated macrophages but without significantly increasing the infiltration of CD8<sup>+</sup> T cells. Our findings suggest that SIX2 is a potential key player in CC, offering insights into future research and the development of targeted therapies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"772 ","pages":"Article 152038"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130911","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

Glycyrrhetinic acid triggers lipid peroxidation-related cell death in tobacco BY-2 cells 甘草次酸触发烟草BY-2细胞脂质过氧化相关细胞死亡

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-21 DOI: 10.1016/j.bbrc.2025.152062

Kazuma Hirase , Takumi Higaki

{"title":"Glycyrrhetinic acid triggers lipid peroxidation-related cell death in tobacco BY-2 cells","authors":"Kazuma Hirase , Takumi Higaki","doi":"10.1016/j.bbrc.2025.152062","DOIUrl":"10.1016/j.bbrc.2025.152062","url":null,"abstract":"<div><div>Glycyrrhetinic acid (GA), a triterpenoid saponin from licorice (<em>Glycyrrhiza</em> species) exerts diverse biological activities in animal cells, including anti-inflammatory, antiviral, and antitumor effects. However, the effects of GA on plant cells remain largely unexplored. In this study, we investigated the effects of GA on tobacco BY-2 cells, a plant cell culture system that serves as a useful model for studying cell death in highly proliferative plant cells. Treatment of BY-2 cells with GA resulted in a significant increase in cell death in a manner dependent on both concentration and time. To elucidate the mechanisms underlying GA-induced cell death, we evaluated mitochondrial membrane potential and lipid peroxidation using fluorescent probes. GA treatment caused a marked decrease in mitochondrial membrane potential, along with an increase in lipid peroxidation levels. These findings suggest that GA induces cell death in plant cultured cells, accompanied by mitochondrial dysfunction and lipid peroxidation. Our results provide new insights into the biological activity of GA in plant cells and suggest the involvement of mitochondrial and lipid peroxidation-related pathways in GA-induced cell death.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"772 ","pages":"Article 152062"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144131397","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

Endolysosomal engulfment of autophagosomes independent of ESCRT 独立于ESCRT的自噬体的内溶酶体吞噬

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2025-05-21 DOI: 10.1016/j.bbrc.2025.152060

Rui Tian , Zhe Wu , Yufen Wang , Chuangpeng Li , Fengping Liu , Yueguang Rong

引用次数: 0