Biochemical and biophysical research communications最新文献

{"title":"Mechanistic insights into molecular targeted therapy and immunotherapy for lung cancer","authors":"Teresa Vincent ,&nbsp;Kunnathur Murugesan Sakthivel ,&nbsp;C.M. Reena Josephine ,&nbsp;Roopa Prasad ,&nbsp;Kathirvelan Chinnadurai ,&nbsp;Pavithra Kumar ,&nbsp;Mythili Saravanan ,&nbsp;Rajan Radha Rasmi","doi":"10.1016/j.bbrc.2025.152204","DOIUrl":"10.1016/j.bbrc.2025.152204","url":null,"abstract":"<div><div>Lung cancer is a serious public health concern and a leading cause of cancer related deaths worldwide. The major drawback of conventional therapies such as chemotherapy, radiotherapy, and surgery is their limited efficacy and lack of tumor specificity. Of these treatment options, targeted therapy and immunotherapy are of best interest due to their potential to selectively target cancer cells and enhance immune responses. Targeted therapy can bind to molecular targets and inhibit pathways involved in cell growth, proliferation, and survival. In the case of lung cancer, targeting expressions of EGFR, KRAS, and BRAF are important as their overexpression makes up a significant portion of cancer cases. Targets in the MAPK, PI3K, and MYC pathway are also inhibited as each of these pathways promote cell proliferation and growth. Immunotherapy directly kills off cancerous cells by amplifying the behavior of immune cells. Immunotherapeutic targets include NK-cells, T-cells, and immune checkpoints. NK cells and T cells are involved in the elimination of cancer cells, while immune checkpoints regulate the immune system but may be exploited by cancerous cells. The advent of molecular targeted therapy and immunotherapy has significantly transformed lung cancer treatment, offering precision and efficacy in combating tumor resistance. Their integration in combination strategies holds great promise for improved clinical outcomes and represents a pivotal direction for future therapeutic advancements.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152204"},"PeriodicalIF":2.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307319","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":"Study of antitumor efficacy and pharmacokinetics of a photosensitizer based on natural furanocoumarins and upconversion rare earth metal particles in mice with Lewis lung carcinoma and B16 melanoma","authors":"Vasilisa I. Shlyapkina ,&nbsp;Mikhail N. Zharkov ,&nbsp;Denis E. Yakobson ,&nbsp;Nikolay A. Pyataev ,&nbsp;Ekaterina S. Prikhozhdenko ,&nbsp;Alexey A. Burtasov ,&nbsp;Olga I. Balakireva ,&nbsp;Irina A. Gololobova ,&nbsp;Anna A. Gadeeva ,&nbsp;Vladislav S. Bobrov ,&nbsp;Oleg A. Kulikov","doi":"10.1016/j.bbrc.2025.152202","DOIUrl":"10.1016/j.bbrc.2025.152202","url":null,"abstract":"<div><div>In this work, the phototherapeutic potential of a photosensitizer containing natural furanocoumarins and upconversion microparticles NaYF₄:20 %Yb,0.25 %Tm, possessing UV luminescence, was investigated on an <em>in vivo</em> tumor growth model.</div><div>The study included an assessment of the antitumor efficacy, pharmacokinetics and biophysical properties of the photosensitizer in mice with malignant neoplasm models (Lewis lung carcinoma and B16 melanoma).</div><div>As a result of the study, a liquid form of the experimental photosensitizer was developed, which is an emulsion of furanocoumarins from the <em>Heracleum sosnowskyi</em> plant, which contained microparticles of NaYF₄:20 %Yb,0.25 %Tm (EmFHS-UCPs).</div><div>The results of the study of the pharmacokinetics of organic and inorganic components of the EmFHS-UCPs photosensitizer substantiate the use of the intratumoral route of administration in experimental phototherapy.</div><div>In mice with transplantable Lewis lung carcinoma, intratumoral injection of EmFHS-UCPs followed by laser irradiation (λ-980 nm) was shown to result in inhibition of tumor growth, tumor nodule reduction, and increased survival of tumor-bearing animals.</div><div>No antitumor effect was detected in mice with B16 melanoma.</div><div>An <em>ex vivo</em> study using tissues from experimental animals substantiated the biophysical reasons affecting the success of antitumor phototherapy using UV (365 nm) and IR (980 nm) radiation.</div><div>The study showed that the degree of antitumor efficacy of emulsion furanocoumarins containing NaYF₄:20 %Yb,0.25 %Tm microparticles directly depends on the optimal route of photosensitizer administration and optical properties of tumor tissues.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152202"},"PeriodicalIF":2.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144297099","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":"Loss of DNA replication fork protection by TIMELESS degradation supports oncogene-induced senescence","authors":"Jennifer J. Park ,&nbsp;Julie Rageul ,&nbsp;Natalie Lo ,&nbsp;Jinal A. Patel ,&nbsp;Flaminia Talos ,&nbsp;Hyungjin Kim","doi":"10.1016/j.bbrc.2025.152203","DOIUrl":"10.1016/j.bbrc.2025.152203","url":null,"abstract":"<div><div>Oncogene-induced senescence (OIS) is a potent barrier that limits tumorigenesis. While persistent DNA replication stress accompanied by cellular hyperproliferation is considered an underlying basis of OIS, the molecular mechanisms through which oncogenes elicit genome instability remain unclear. Here, we identify a distinct cellular process in which DNA replication fork stalling is linked to senescence in response to oncogenic signaling. We demonstrate that TIMELESS (TIM), an essential regulatory component of the fork protection complex that supports the integrity of the replisome, is downregulated in non-transformed human cell lines that undergo OIS by HRAS^G12V expression. Loss of TIM is sufficient to induce senescence, while ectopic expression of TIM delays the induction of OIS via enhancing protection of stalled forks. Furthermore, TIM levels are restored in cells capable of bypassing OIS, indicating that TIM regulation modulates the onset of OIS. Mechanistically, HRAS^G12V expression induces cellular poly(ADP-ribosyl)ation mediated by PARP1, which prompts poly(ADP-ribose)/PAR-dependent TIM degradation. Together, our study uncovers RAS-mediated proteolytic signaling as a key determinant of OIS centered at stalled DNA replication forks. We propose the existence of an oncogenic signaling cascade that actively suppresses replisome activity, contributing to the DNA replication stress that drives OIS.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152203"},"PeriodicalIF":2.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144288738","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":"AP1S3 affects lipid metabolism in breast cancer cells by regulating the PI3K/AKT/mTOR pathway","authors":"Zankai Wu ,&nbsp;Shanshan Wang ,&nbsp;Qingfeng Yang ,&nbsp;Yiping Gong ,&nbsp;Jin Hu","doi":"10.1016/j.bbrc.2025.152200","DOIUrl":"10.1016/j.bbrc.2025.152200","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to investigate the role of adaptor protein complex 1 sigma 3 (AP1S3) in breast cancer (BRCA) progression, focusing on its regulatory effects on lipid metabolism and the PI3K/AKT/mTOR signaling pathway.</div></div><div><h3>Methods</h3><div>AP1S3 expression levels in BRCA cells were analyzed using the TCGA transcriptome database, with associated pathways identified through GO and KEGG analyses. The effects of AP1S3 on BRCA cell (MDA-MB-231 and MDA-MB-436) proliferation and migration were detected using CCK-8, colony formation, wound healing, and Transwell migration assays. Additionally, the regulatory effect of AP1S3 on lipid metabolism in BRCA cells was evaluated by measuring lipid droplet accumulation, free fatty acid (FFA) levels and total cholesterol (TC) content.</div></div><div><h3>Results</h3><div>AP1S3 was significantly upregulated in BRCA cells and correlated with poor patient prognosis. Functional studies demonstrated that AP1S3 knockdown substantially inhibited BRCA cell proliferation and migration. Mechanistically, AP1S3 facilitated lipid metabolism and tumor progression by activating the PI3K/AKT/mTOR pathway. AP1S3 silencing resulted in decreased lipid accumulation and downregulation of lipid metabolism-related genes.</div></div><div><h3>Conclusion</h3><div>This study highlights the crucial involvement of AP1S3 in BRCA progression through its modulation of lipid metabolism and the PI3K/AKT/mTOR pathway. These findings suggest that targeting AP1S3 could provide novel insights and therapeutic avenues for treating metastatic BRCA.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152200"},"PeriodicalIF":2.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144338399","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":"Identification of epithelial membrane protein 3 as a novel biomarker in Alzheimer's disease that involves in amyloid-β-induced inflammatory response","authors":"Sisi Deng ,&nbsp;Yuqing Zhao ,&nbsp;Wenjing Yu ,&nbsp;Miao Yang ,&nbsp;Chunxiang He ,&nbsp;Ze Li ,&nbsp;Jiawei He ,&nbsp;Zhenyan Song ,&nbsp;Yi Zang ,&nbsp;Shaowu Cheng","doi":"10.1016/j.bbrc.2025.152183","DOIUrl":"10.1016/j.bbrc.2025.152183","url":null,"abstract":"<div><div>Chronic neuroinflammation is a major contributor to neuronal dysfunction and neurodegeneration in Alzheimer's disease (AD), the most prevalent neurodegenerative disorder worldwide. In this study, bioinformatic analyses identified differentially expressed inflammatory response genes across multiple AD-affected brain regions. Among these, epithelial membrane protein 3 (EMP3), a putative regulator of macrophage and T cell immune responses, was found to be dysregulated in both human AD brain tissues and in AD animal models, including 3 × Tg-AD mice. Functional validation using CRISPR-Cas9-mediated EMP3 knockout in SH-SY5Y neuroblastoma cells demonstrated that EMP3 deletion attenuated Aβ-induced suppression of cell proliferation and apoptosis. Western blot analysis further revealed a reduction in GSK3β phosphorylation in EMP3-deficient cells following Aβ exposure, possibly by effected its upstream regulator. Notably, GSK3β overactivation has been associated with memory impairment, tau hyperphosphorylation, and enhanced Aβ production in AD. Transcriptomic profiling via RNA sequencing uncovered altered expression of several inflammatory genes involved in the downstream response to Aβ, including key regulators such as <em>TLR2</em>, <em>S100A10</em>, and <em>CD44</em>. The association between EMP3 and inflammatory pathways was further supported by weighted gene co-expression network analysis (WGCNA) and immune infiltration analysis. Collectively, these findings suggest that EMP3 may serve as a critical modulator of neuroinflammatory processes in AD pathogenesis and highlight its potential as a therapeutic target for future interventions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152183"},"PeriodicalIF":2.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144321763","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":"Validated target-based network pharmacology reveals that salvianolic acid C attenuates doxorubicin-induced cardiotoxicity by regulating apoptosis and oxidative stress","authors":"Siqi Chen ,&nbsp;Chenchen Jiang ,&nbsp;Xiaojiao Yi ,&nbsp;Qi Shu ,&nbsp;Yan Feng ,&nbsp;Like Zhong ,&nbsp;Min Huang ,&nbsp;Junfeng Zhu ,&nbsp;Luo Fang","doi":"10.1016/j.bbrc.2025.152196","DOIUrl":"10.1016/j.bbrc.2025.152196","url":null,"abstract":"<div><div>Doxorubicin (DOX), an anthracycline commonly used to treat various cancers, is associated with irreversible and dose-dependent cardiotoxicity. Salvianolic acid C (SAC) is a major polyphenolic compound in <em>Salvia miltiorrhiza,</em> an herbal medicine with significant cardioprotective effects. However, the role and mechanism of SAC in protecting against DIC remain unreported. Therefore, this study aims to investigate the protective effects and mechanisms of action of SAC against DOX-induced cardiotoxicity (DIC) through validated target-based network pharmacology. <em>In vitro</em> experiments using H9c2 cells revealed that SAC attenuated DOX-induced cardiomyocyte injury. Network pharmacology analysis revealed that apoptosis and oxidative stress play vital roles in mediating the protective effects of SAC against DIC. TUNEL staining and flow cytometry revealed that SAC inhibited DOX-induced apoptosis. Additionally, SAC mitigated DOX-induced oxidative stress by regulating the levels of reactive oxygen species, malondialdehyde, superoxide dismutase, and glutathione. Western blotting analysis revealed that SAC inhibited DOX-induced oxidative stress by reducing JNK phosphorylation, enhancing PI3K-AKT-mTOR pathway activation, and upregulating the antioxidant factors Nrf2 and HO-1. Furthermore, the reduction in cleaved caspase-3 and the increase in the Bcl-2/Bax ratio confirmed the inhibitory effect of SAC on apoptosis. Together, based on validated targets, these findings provide the first elucidation that SAC attenuates DIC by inhibiting apoptosis and oxidative stress through the regulation of the PI3K-AKT/JNK pathway, highlighting its potential for subsequent cotreatment with DOX in clinical applications.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"775 ","pages":"Article 152196"},"PeriodicalIF":2.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144271140","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":"Vascular mimicry developments in non-small cell lung cancer","authors":"Xiaoyou Zhong ,&nbsp;Yiteng Gao ,&nbsp;Jiajia Lv,&nbsp;Weifei Fan,&nbsp;Lin Wang","doi":"10.1016/j.bbrc.2025.152195","DOIUrl":"10.1016/j.bbrc.2025.152195","url":null,"abstract":"<div><div>Non-small cell lung cancer (NSCLC) remains a prevalent and lethal malignancy worldwide, posing significant challenges in therapeutic management. The limited clinical effectiveness of conventional antiangiogenic therapies in NSCLC is mainly attributed to vasculogenic mimicry (VM), an atypical angiogenic mechanism observed in tumors. VM involves tumor cells transforming into vascular-like channels, advancing tumor progression by providing essential nutrients and oxygen. These structures, formed by tumor cells instead of endothelial cells, are resistant to traditional antiangiogenic drugs targeting vascular endothelial growth factor (VEGF) pathways, allowing tumors to evade suppression by standard antivascular treatments and significantly contributing to therapeutic resistance. Therefore, a thorough investigation of VM formation mechanisms, its regulatory pathways, and the association between VM formation mechanisms and prognosis in NSCLC has both theoretical and clinical significance for developing innovative therapeutic strategies and improving patient survival.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152195"},"PeriodicalIF":2.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279794","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":"Retraction notice to \"Identification of an antitumor immune response of polyhistidine through a toll-like receptor 4-dependent manner\" [Biochem. Biophys. Res. Commun. 453 (2014) 148-152 32760].","authors":"Feng Wang, Yong Yang","doi":"10.1016/j.bbrc.2025.152153","DOIUrl":"https://doi.org/10.1016/j.bbrc.2025.152153","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"152153"},"PeriodicalIF":2.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282319","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":"NHE9 regulates exosomal stress response to hypoxia in cardiomyocytes","authors":"Lili A. Hafezi,&nbsp;Mariam Duhaini,&nbsp;Kalyan C. Kondapalli","doi":"10.1016/j.bbrc.2025.152191","DOIUrl":"10.1016/j.bbrc.2025.152191","url":null,"abstract":"<div><div>Hypoxia, a major stressor in conditions like ischemia, significantly impacts the function and communication of cardiomyocytes. Cells adapt to hypoxia through various mechanisms, including the release of exosomes. Exosomes are nanoscale vesicles that facilitate intercellular signaling by transferring specific biomolecular cargos. Despite this understanding, the molecules driving these stress responses and the release of exosomes remain unclear. Recent research efforts are focused on identifying the key molecular players involved in exosome release during hypoxic conditions to gain a clearer understanding of these adaptive mechanisms. The endosomal sodium-proton exchanger NHE9 was recently identified as a crucial regulator of exosome biogenesis. In this study, we used human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) and H9c2, a mouse cardiomyocyte cell line as models to show that hypoxia leads to significant upregulation of NHE9. To investigate the role of NHE9 upregulation during hypoxia, we generated genetically engineered cell lines with altered NHE9 expression. We then examined exosome dynamics under hypoxic conditions in cell lines where NHE9 was either overexpressed or knocked down. Exosomes were isolated and characterized using nanoparticle tracking analysis and Western blotting. Our results demonstrate that NHE9 upregulation leads to a significant increase in exosome secretion and enriches these exosomes with stress response proteins, specifically hypoxia-inducible factor 1-alpha (HIF1α) and heat shock protein 70 (Hsp70). Therefore, this study reveals a novel role for NHE9 as a critical regulator of stress signaling in hypoxic environments, offering new insights into cardiomyocyte adaptation and potential therapeutic interventions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"776 ","pages":"Article 152191"},"PeriodicalIF":2.5,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144270600","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":"Retraction notice to \"Inhibition of PKM2 sensitizes triple-negative breast cancer cells to doxorubicin\" [Biochem. Biophys. Res. Commun. 454 (2014) 465-470 32936].","authors":"Feng Wang, Yong Yang","doi":"10.1016/j.bbrc.2025.152154","DOIUrl":"10.1016/j.bbrc.2025.152154","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"152154"},"PeriodicalIF":2.5,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274132","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}