Biochemical and biophysical research communications最新文献

{"title":"Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood","authors":"Timra Gilson ,&nbsp;Jacob W. Astroski ,&nbsp;Wang Qun ,&nbsp;Matthew J. Turner ,&nbsp;Elliot J. Androphy ,&nbsp;Sara K. Custer","doi":"10.1016/j.bbrc.2025.152201","DOIUrl":"10.1016/j.bbrc.2025.152201","url":null,"abstract":"<div><div>The COPI coatomer is a heptameric complex that regulates traffic between the Golgi apparatus and the Endoplasmic Reticulum (ER). Mutations in the <em>COPA</em> gene encoding the alpha subunit of the COPI complex result in an autoimmune disorder impacting multiple tissues including the lungs, joints, and kidneys. We report here the characterization of a conditional-ready <em>Copa</em> knockout mouse. Systemic homozygous deletion of <em>Copa</em> in mice resulted in embryonic lethality. Deletion of <em>Copa</em> in Chat-positive cells also resulted in late embryonic lethality. However, the deletion of <em>Copa</em> by Cre recombinase expression under the Mnx1 promoter was compatible with development and viability. In adulthood, these mice display a modest glucose intolerance, most likely due to Mnx1-driven pancreatic expression of Cre recombinase. Systemic deletion of <em>Copa</em> in adult mice results in rapid decline and death. Lung fibroblasts cultured from mice expressing a Tamoxifen-inducible Cre recombinase demonstrate robust <em>Copa</em> knockout, resulting in near complete loss of alpha-COP protein. These cultures recapitulate the previously described COPA syndrome phenotype, including hyperactivation of STING (Stimulator of Interferon Genes) signaling and induction of ER stress. Dorsal Root Ganglion neurons cultured from Tamoxifen-inducible <em>Copa</em> knockout mice show that axonal arbor maintenance and viability requires <em>Copa</em> expression.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152201"},"PeriodicalIF":2.5,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144365309","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}

{"title":"Estrogen deficiency impairs double-negative T cell function and activates NF-κB in postmenopausal osteoporosis","authors":"Hua Jin ,&nbsp;Mengmeng Chen ,&nbsp;Xiyu Wang ,&nbsp;Guangyong Sun ,&nbsp;Hao Chen ,&nbsp;Dong Zhang","doi":"10.1016/j.bbrc.2025.152212","DOIUrl":"10.1016/j.bbrc.2025.152212","url":null,"abstract":"<div><div>Postmenopausal osteoporosis (PMOP), which is driven primarily by estrogen deficiency, is characterized by excessive bone resorption and disrupted immune homeostasis. Although immune system contributions to bone loss are well-documented, the roles of specific regulatory subsets, such as double-negative T (DNT) cells (CD3⁺TCRαβ⁺CD4⁻CD8⁻NK1.1⁻), remain unclear. Herein, by using an ovariectomized (OVX) mouse model of PMOP, we integrated transcriptomic profiling, <em>in vivo</em> functional assays, and <em>in vitro</em> studies to investigate DNT cell alterations. The OVX mice presented significant reductions in both DNT cell frequency and immunoregulatory capacity, which were accompanied by their increased apoptosis and suppressed proliferation. RNA sequencing revealed concurrent upregulation of NF-κB signaling and apoptotic pathways with downregulation of estrogen receptor (ER) signaling and cytotoxicity. <em>In vitro</em>, estrogen stimulation enhanced DNT cell immunoregulatory function and estrogen receptor <em>Esr1</em> expression, while inhibiting NF-κB activation. These results demonstrated that estrogen deficiency impaired DNT cell viability and function, potentially through NF-κB pathway activation, thereby exacerbating immune dysregulation in PMOP. Our study suggests that DNT cells may represent important immune players involved in osteoimmunology and potential targets for immunomodulatory therapies of osteoporosis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152212"},"PeriodicalIF":2.5,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306853","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}

{"title":"Mechanical stimulation induces electrical coupling via TNTs through calcium-dependent mechanisms in C2C12 cells","authors":"Yanli Sun ,&nbsp;Hucheng Zhao","doi":"10.1016/j.bbrc.2025.152186","DOIUrl":"10.1016/j.bbrc.2025.152186","url":null,"abstract":"<div><div>Intercellular communication and cellular material exchange are essential for the development, tissue repair, and survival of multicellular organisms. Tunneling nanotubes (TNTs) serve as long-distance intercellular connections that facilitate the transmission of biochemical and electrical signals between cells. However, the mechanisms underlying this process remain largely unknown. This study uses mechanical stimulation to explore the transmission and mechanisms of mechano-electrical signals mediated by TNTs. We assessed both gap junction (GJ)-mediated and TNT-mediated intercellular electrical coupling in HEK cells, A549 cells, and C2C12 cells. Our results show that the coupling ratio was lower in HEK cells compared to A549 cells, with the highest ratio observed in C2C12 cells. Additionally, the strength of TNT-mediated electrical coupling decreased as TNT length increased. Using C2C12 cells as a model, we found that Ca²⁺ influx and the gap junction protein Connexin 43 (Cx43) play roles in TNT-mediated electrical coupling induced by mechanical stimulation. Mechanical stimulation triggers extracellular Ca²⁺ entry into C2C12 cells via mechanosensitive and T-type calcium channels. Our experiments also demonstrate that TNT-mediated electrical coupling between C2C12 cells is predominantly unidirectional. These findings provide new insights into the mechanisms of intercellular electrical signal transmission.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152186"},"PeriodicalIF":2.5,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306858","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}

{"title":"Deciphering the transcriptomic characteristic of lactate metabolism and the immune infiltration landscape in abdominal aortic aneurysm","authors":"Min Zhang ,&nbsp;Ru Ying ,&nbsp;Song Lu","doi":"10.1016/j.bbrc.2025.152198","DOIUrl":"10.1016/j.bbrc.2025.152198","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Abdominal aortic aneurysm (AAA) is a common degenerative vascular disease characterized by progressive dilation of the abdominal aorta, which poses a life-threatening risk upon rupture. Lactate, a key metabolic byproduct and immunomodulatory molecule, plays a crucial role in regulating immune cell functions in various inflammatory diseases. However, the specific involvement of lactate metabolism in the pathogenesis of AAA remains poorly understood. This study aims to identify lactate metabolism-related gene signatures associated with AAA and to elucidate their potential roles and underlying mechanisms in disease progression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Transcriptomic datasets GSE57691, GSE183464, and GSE237230 were obtained from the Gene Expression Omnibus (GEO) database. Lactate metabolism-related genes were retrieved from the Molecular Signatures Database (MSigDB). Weighted Gene Co-expression Network Analysis (WGCNA) and the Limma R package were employed to identify key gene modules associated with AAA and detect differentially expressed genes (DEGs) between AAA and control groups, respectively. Overlapping genes were subjected to functional enrichment analysis and protein–protein interaction (PPI) network construction. Three distinct machine learning algorithms were applied to screen for potential diagnostic biomarkers. Upon validation, a nomogram was constructed based on the selected biomarkers. Immune infiltration and single-cell RNA analysis were performed to characterize the immune microenvironment and investigate the association between immune cell subsets and AAA-related biomarkers. Finally, the expression patterns of the identified biomarkers were validated using a murine model of AAA.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;A total of 3336 AAA-related module genes, 2651 DEGs between AAA and controls, and 364 lactate metabolism-related genes were identified. Among these, 29 genes were recognized as lactate metabolism-related DEGs associated with AAA. Functional enrichment analysis revealed significant enrichment in pathways related to oxidative phosphorylation and energy metabolism. SLC25A4, HBB, and STAT4 were identified as candidate biomarkers for AAA. Immune infiltration analysis revealed distinct immune profiles between AAA and control groups. Single-cell mRNA analysis demonstrated that SLC25A4 is predominantly expressed in adventitial cells and fibroblasts in AAA, HBB is expressed across multiple immune cell subsets, and STAT4 is mainly expressed in T cells. Gene Set Enrichment Analysis indicated that these biomarkers are involved in biological processes related to T cell activation and T cell differentiation. These findings were further validated in a murine model of AAA.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;The identification of lactate metabolism-related biomarkers and the comprehensive characterization of the immune microenvironment in AAA offer novel insights that may contribute to the de","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152198"},"PeriodicalIF":2.5,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307318","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}

{"title":"Hippocampal transcriptome profiling associated with post-traumatic stress disorder-like behaviors in male mice","authors":"Zhen He ,&nbsp;Yihan Qin ,&nbsp;Guanbo Xie ,&nbsp;Fei Li ,&nbsp;Ning Wu","doi":"10.1016/j.bbrc.2025.152205","DOIUrl":"10.1016/j.bbrc.2025.152205","url":null,"abstract":"<div><div>Post-traumatic stress disorder (PTSD) is a trauma- and stressor-related disorder characterized by re-experiencing, avoidance of trauma-related stimuli, negative changes in mood and cognition, and hyperarousal. Despite its prevalence, the pathogenesis and molecular mechanisms underlying PTSD remain poorly understood. In the present study, a mouse model simulating PTSD was established through a modified single prolonged stress (SPS) in conjunction with plantar shock (SPS+shock). Contextual fear-like and active avoidance behaviors were assessed using the contextual freezing test and the cue avoidance test, respectively. Four weeks after stress exposure, the SPS+shock mice were categorized into PTSD-like (+) (exhibiting PTSD-like behavioral phenotype) and PTSD-like (-) (lacking the behavioral phenotype) groups. Hippocampal gene expression profiles were obtained through high-throughput RNA sequencing (RNA-seq). Functional enrichment analysis of significantly differentially expressed genes revealed pathways associated with the PTSD-like (+) phenotype, including the Notch signaling pathway and GABAergic synapse. Using the CytoHubba plugin, three hub genes enriched in the Notch signaling pathway and three hub genes enriched in the GABAergic synapse were identified. Additionally, weighted gene co-expression network analysis highlighted key pathways, including the Notch signaling pathway, ATP-dependent chromatin remodeling, histone modification and mitochondrial oxidative phosphorylation. Within these pathways, 16 hub genes were screened out. Additionally, the mRNA expression changes of nine hub genes validated by qPCR, showed similar trends to the RNA-seq data. Collectively, our results found important biological pathways and hub genes associated with the PTSD-like behavioral phenotype in mice, offering potential insights into the pathological mechanisms of PTSD and identifying novel therapeutic targets.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152205"},"PeriodicalIF":2.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144314387","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}

{"title":"Ultrasound-targeted microbubble destruction mediated upregulation of CNN1 induces ferroptosis in colorectal cancer cells by regulating p53-related SLC7A11 expression","authors":"Lingxiao Wang ,&nbsp;Wenjing Wang ,&nbsp;Shuang Wu ,&nbsp;Yixiang Shi","doi":"10.1016/j.bbrc.2025.152207","DOIUrl":"10.1016/j.bbrc.2025.152207","url":null,"abstract":"<div><div>Colorectal cancer (CRC) represents a leading cause of cancer-related mortality, with patients often demonstrating suboptimal responses to current therapeutic modalities, underscoring the need for innovative treatment therapies. Ultrasound-targeted microbubble destruction (UTMD) has emerged as a promising technique to enhance gene transfection efficiency. While previous research has established the critical role of CyclinD1 (CNN1) in the pathogenesis of multiple cancer types, its involvement in CRC progression remains underinvestigated. In this study, we sought to elucidate the impact of UTMD-mediated CNN1 modulation on CRC progression. In the present study, data indicate that CNN1 is underexpressed in CRC and may contribute to CRC progression. UTMD-assisted transfection of CNN1 exhibits significantly higher efficiency compared to liposomes (LIP)-mediated transfection. UTMD-mediated CNN1 overexpression potently inhibits CRC cell proliferation and promotes cell apoptosis. Mechanistic investigations reveal that UTMD-drivenCNN1 overexpression suppresses CRC cell proliferation via the p53 signaling pathway. Further studies confirm that SLC7A11 is overexpressed in CRC tissues, whereas CNN1 overexpression downregulates SLC7A11 expression. Notably, p53 inhibits SLC7A11 transcription by directly binding to its promoter region. Rescue experiments demonstrate that UTMD-mediated CNN1 overexpression induces ferroptosis through activation of the p53-SLC7A11 pathway. Collectively, UTMD-driven upregulation of CNN1 elicits ferroptosis in CRC cells by modulating p53-associated SLC7A11 expression. These findings highlight CNN1 as a potential target for therapeutic intervention and diagnostic strategies in CRC.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152207"},"PeriodicalIF":2.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144518079","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}

{"title":"Unraveling the mechanism of RNA duplex unwinding by DEAD-box helicase DDX3X: Insights into Cooperativity and roles of protomers","authors":"Sudhaker Dharavath ,&nbsp;He Song ,&nbsp;Xinhua Ji","doi":"10.1016/j.bbrc.2025.152206","DOIUrl":"10.1016/j.bbrc.2025.152206","url":null,"abstract":"<div><div>DDX3X, a human DEAD-box helicase involved in ATP-dependent unwinding of short RNA duplexes, plays a pivotal role in RNA metabolism, cancer progression, and HIV-1 infection. It is composed of an N-terminal region (N: residues 1–131), a helicase core containing two RecA-like domains (D1D2: residues 132–607), and a C-terminal tail (C: residues 608–662). Previous research has shown that D1D2 forms a pre-unwound complex with dsRNA, exhibiting two-molecule cooperativity for both RNA-unwinding and ATPase activities. However, the cooperative mechanism by which the full-length DDX3X (N-D1D2-C) unwinds RNA remains to be fully understood. Knowing that the C-terminal tail is crucial for oligomerization, we have created an N-truncated form of DDX3X (D1D2-C: residues 132–662) for further investigation. Our findings indicate that D1D2-C oligomerizes in the presence of RNA substrate, exhibits three-molecule cooperativity for RNA-unwinding activity, and displays two-molecule cooperativity for ATPase activity. Furthermore, D1 residue E186 and C-terminal tail are essential for the oligomerization of D1D2-C, enabling two types of subunit interface to form, one between two D1 domains (C-D2D1:D1D2-C) and the other between two C-terminal tails (D1D2-C:C-D2D1). These results offer new insights into the molecular mechanism of cooperative RNA unwinding by DDX3X.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152206"},"PeriodicalIF":2.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480267","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}

{"title":"Corrigendum to \"Pirin is a nuclear redox-sensitive modulator of autophagy-dependent ferroptosis\" [Biochem. Biophys. Res. Commun. 536 (2021) 100-106].","authors":"Nanjun Hu, Lulu Bai, Enyong Dai, Leng Han, Rui Kang, Daolin Tang, Hongjun Li","doi":"10.1016/j.bbrc.2025.152158","DOIUrl":"https://doi.org/10.1016/j.bbrc.2025.152158","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"152158"},"PeriodicalIF":2.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293185","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}

{"title":"Dietary gamma-aminobutyric acid enhances endurance exercise capacity through mechanisms involving activation of peroxisome proliferator-activated receptor gamma coactivator-1 alpha","authors":"Maya Sakashita ,&nbsp;Hiroaki Yamada ,&nbsp;Yugweng Kim ,&nbsp;Xuan Li ,&nbsp;Yusuke Yamashita ,&nbsp;Youngil Kim ,&nbsp;Yuki Ito ,&nbsp;Wataru Aoi ,&nbsp;Satoshi Fujita","doi":"10.1016/j.bbrc.2025.152208","DOIUrl":"10.1016/j.bbrc.2025.152208","url":null,"abstract":"<div><div>Dietary gamma-aminobutyric acid (GABA) provides physiological benefits and has been extensively studied for its metabolic effects such as reducing stress, hypertension, improving sleep and cognitive function. However, its effects, when combined with exercise training, on endurance exercise capacity remain unclear. In this study, we aimed to investigate the combined effects of dietary GABA supplementation and exercise training on endurance performance in mice and explore its underlying mechanisms. Mice were divided into four groups: (1) control (standard diet, no training), (2) GABA (GABA-supplemented diet, no training), (3) training (standard diet, treadmill training), and (4) GABA-training (GABA-supplemented diet, treadmill training). Skeletal muscle samples were analyzed for molecular and metabolic changes. The findings demonstrated that dietary GABA supplementation significantly increased the treadmill endurance time, with the most pronounced effect observed in the GABA-training group. Mechanistic analysis revealed that these endurance improvements were associated with enhanced activation of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), glycogen storage, and mitochondrial biogenesis in skeletal muscle. These findings suggest that dietary GABA supplementation enhances exercise-induced adaptations and endurance performance by modulating key metabolic pathways and may serve as a valuable dietary supplement for athletes and physically active individuals seeking to improve endurance capacity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152208"},"PeriodicalIF":2.5,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144329714","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}

{"title":"Dihydroartemisinin restrains angiogenesis through the TNF-α pathway to enhance the efficacy of anti-PD-1 immunotherapy in breast cancer","authors":"Meng Zou ,&nbsp;Yu Gong ,&nbsp;Jiawei Zeng ,&nbsp;Xiyu Zhang ,&nbsp;Xiaohong Guo ,&nbsp;Jianghuan Hua ,&nbsp;Zhuobin Chen ,&nbsp;Li Lin ,&nbsp;Fenghua Wu","doi":"10.1016/j.bbrc.2025.152171","DOIUrl":"10.1016/j.bbrc.2025.152171","url":null,"abstract":"<div><div>Tumor vascular abnormality promotes the formation of immunosuppressive microenvironment, thus limiting the efficacy of tumor immunotherapy and promoting tumor development. Dihydroartemisinin (DHA) has shown potential as an anti-tumor agent. The potential role of its anti-angiogenic effect has not yet been discovered. This research investigates whether DHA inhibits tumor-induced angiogenesis, promotes immunotherapy and explored the underlying mechanism. The promoting effect of 4T-1 cell-conditioned media (CM) on SVEC4-10 activity and tube formation can be reversed by DHA-treated with CM. Consistently, following DHA administration in a breast cancer mouse model, the number of transplanted tumor vessels was markedly reduced and perivascular cells increased. Subsequently, in vivo administration of DHA evidently promoted inhibitory effect of anti-PD-1 in tumor and reversed the infiltration of T cells and the phenotypes of macrophages. Network pharmacology and RNA-seq analysis revealed that DHA inhibit tumor growth by angiogenesis through the TNF-α pathway. Besides, TNF-α cytokine replenishment experiment and the expression of key molecules involved signaling pathway confirmed the above mechanism. In conclusion, DHA alleviates tumor cell-induced abnormal blood vessels through TNF-α pathway, which contributes to the anti-PD-1 efficacy of tumors.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152171"},"PeriodicalIF":2.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144290784","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}