Biochemical and biophysical research communications最新文献

{"title":"Cardiovascular-specific PTH1R activation enhances exercise-induced cardiac remodeling in a mouse model of calcific atherosclerosis.","authors":"Andy Hon, Mimi Lu, Xuesi M Shao, Linda L Demer, Yin Tintut","doi":"10.1016/j.bbrc.2026.153870","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153870","url":null,"abstract":"<p><p>Exercise reduces cardiovascular events, yet its interactions with parathyroid hormone (PTH) and atherosclerotic calcification as well as their combined effects on cardiac remodeling remain unclear. Thus, we tested effects of constitutive activation of the PTH type I receptor (PTH1R) with and without exercise on aortic calcification and cardiovascular remodeling in a mouse model of atherosclerotic calcification. Female Ldlr^{-/-;Tagln-PTH1R} transgenic (Tg) and Ldlr^-/- littermate control (Ctrl) mice were fed a Western diet beginning at 9-10 weeks of age. At age 40 weeks, mice were assigned to sedentary (SED) or treadmill exercise (TM) regimens for 9 weeks. MicroPET/CT and echocardiography were performed at baseline and study completion. By microCT, aortic calcium content increased in all four groups. However, ¹⁸F-NaF uptake, reflecting mineral surface area, increased only in Ctrl/TM mice. Systolic function improved and left ventricular (LV) mass decreased in Tg/TM and Ctrl/TM groups. However, in Ctrl/TM mice, LV chamber diameter increased while anterior wall thickness decreased, consistent with eccentric remodeling. In contrast, in Tg/TM mice, diastolic wall thickness decreased without chamber enlargement, indicating preserved geometry and enhanced contractile efficiency. In sedentary mice (Tg/SED and Ctrl/SED), diastolic LV diameter increased without changes in wall thickness or systolic function, consistent with ventricular remodeling due to aortic stiffening in hyperlipidemia. These findings suggest that vascular PTH1R signaling selectively modulates cardiovascular adaptation to exercise. By preserving geometry and improving contractile efficiency, PTH1R activation augments the beneficial effects of exercise on adverse cardiac remodeling in atherosclerotic calcification, supporting endocrine and exercise contributions to ventricular-vascular coupling.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153870"},"PeriodicalIF":2.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810218","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":"On proline isomerization and 3D-domain-swapping.","authors":"Ramu Manjula, Naren Chockalingam, Ramaswamy Subramanian, Shachi Gosavi","doi":"10.1016/j.bbrc.2026.153872","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153872","url":null,"abstract":"<p><p>3D-domain-swapping is the exchange of identical \"domains\" between two protein monomers, which leads to homodimerization. This domain exchange can be facilitated by a single hinge-loop extending out. Hinge-loop prolines have been associated with domain-swapping, but their role remains unclear. Previously, we had engineered three domain-swapping variants of the monomeric monellin by replacing the wild-type hinge-loop sequence (L1:YENEGFREIKG) with QEVKG, YEIKG or QVVAG. The central residues of these sequences are hydrophobic (V/I), and lie at the apex of a tight solvent-exposed hinge-loop (L1Δ6) connecting two β-strands (β2-β3). The hydrophobic residue-solvent interaction likely impedes the closure of L1Δ6 and the formation of intra-chain β2-β3 contacts. This promotes domain-swapping. Here, we replaced the apex residue with the borderline-hydrophobic proline and found that it reduced domain-swapping in all three variants, with significant domain-swapping observed only in the most hydrophobic QVPAG construct. We then structurally characterized three monomeric (QEPKG, YEPKG, and QVPAG) and one domain-swapped dimeric (QVPAG) variants of monellin using X-ray crystallography. Interestingly, we find that the dimer has a trans-proline isomer, whereas all three monomers have a cis-proline. Thus, introducing proline into a solvent-exposed tight β-turn may be a robust method for designing cis-proline. Conversely, mutating such a naturally-occurring cis-proline to a hydrophobic amino acid may induce domain-swapping. The trans-proline in a hydrophobic hinge-loop (e.g. QVPAG), can provide rigidity to the domain-swapped dimer enabling the precise design of domain-swapping-driven protein assemblies. Overall, our mutational-design strategy is a step towards clarifying the role of prolines in 3D-domain-swapping and the rational design of proline isomerization.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153872"},"PeriodicalIF":2.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855635","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":"Integrated single-cell transcriptomics and in vivo investigation reveal the role of ANXA1 in intestinal barrier dysfunction during heat stroke by mediating neutrophil-monocyte interaction and regulating the TLR4/ERK/NF-κB pathway.","authors":"Jun Li, Xuemei Chen, Zewen Tong, Yishun Jin","doi":"10.1016/j.bbrc.2026.153873","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153873","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Heat stroke (HS) causes high mortality via multiple organ dysfunction syndrome, with intestinal barrier dysfunction as an early trigger of systemic inflammation. However, the roles of annexin A1 (ANXA1) in HS-induced intestinal barrier dysfunction remain unclear. Therefore, this study investigated the roles of ANXA1 in HS-induced intestinal barrier dysfunction through integrating single-cell transcriptomics and in vivo experiments. The single-cell RNA sequencing (scRNA-seq) data were used to analyze the cell subpopulation changes between healthy controls and HS patients, as well as between the inflammatory sites and non-inflammatory sites in inflammatory bowel disease. In vivo, the H&E staining, flow cytometry, ELISA, and Western blot were used to determine the pathological injuries, the proportion of neutrophils and monocytes, inflammatory cytokine levels, and related protein expression levels in the colon tissue. Immunofluorescence co-localization analysis was performed to detect the interaction between ANXA1 and immune cells. The scRNA-seq data showed that the proportion of neutrophil and CD14&lt;sup&gt;+&lt;/sup&gt;Mono subpopulations was increased in HS patients. Concurrently, the ANXA1 expression was significantly upregulated in multiple immune cell subpopulations, including the CD14&lt;sup&gt;+&lt;/sup&gt;Mono, CD16&lt;sup&gt;+&lt;/sup&gt;Mono, mDC, MDSC, and neutrophil subpopulations. Cell-cell communication analysis further demonstrated that the ANXA1-formyl peptide receptor 2 (FPR2) ligand-receptor pairs were the dominant mode of interaction during HS. Importantly, there was partial overlap between cell populations expressing ANXA1 and barrier genes. In addition, ANXA1 was positively associated with M2 monocyte phenotype in both inflammatory and non-inflammatory sites. After establishing the HS model, there were some alterations in the colon tissue, including the exacerbated pathological injuries, upregulated ANXA1 and FPR2 protein expression levels, downregulated ZO-1 and occludin protein expression levels, increased inflammatory cytokine levels, and activated TLR4/ERK/NF-κB pathway. Immunofluorescence co-localization analysis revealed that the mean density of ANXA1, CD14&lt;sup&gt;+&lt;/sup&gt;, and Ly6G in the colon tissue of HS mice was significantly elevated compared with the control group, and the co-localization of ANXA1 with CD14&lt;sup&gt;+&lt;/sup&gt; and ANXA1 with Ly6G was enhanced. The treatment of Boc1 led to a dramatic reduction in ANXA1 mean density, a further increase in CD14&lt;sup&gt;+&lt;/sup&gt; and Ly6G mean density, and a reduction in the co-localization of ANXA1 with CD14&lt;sup&gt;+&lt;/sup&gt; and Ly6G. Apart from reversing the ANXA1 and FPR2 protein expression levels, inhibiting ANXA1 aggravated the damaging effects of HS on the colon tissue. In conclusion, ANXA1 protected against HS-induced intestinal barrier dysfunction by regulating neutrophil-monocyte interaction and inhibiting TLR4/ERK/NF-κB, with ANXA1-FPR2 as a key axis, which offers a novel target and strategy for the clinical t","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153873"},"PeriodicalIF":2.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810244","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":"Low concentrations of sorafenib increase dihydrosphingomyelin during antifibrotic processes in human hepatic stellate cells.","authors":"Yeonseo Kim, Baknoon Ham, Yeojin Kim, Byung Hwa Jung, Jinyoung Park, Hyunbeom Lee","doi":"10.1016/j.bbrc.2026.153785","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153785","url":null,"abstract":"<p><strong>Background: </strong>Inhibiting hepatic stellate cells (HSCs) activation, which represents the initial step of liver fibrosis, is a key strategy for fibrosis treatment. Sorafenib has been repurposed as an antifibrotic agent; however, its reported effects largely rely on cytotoxic mechanisms. The antifibrotic mechanisms induced by minimally cytotoxic sorafenib remain unclear. We aimed to elucidate the dynamic changes in gene expression and lipid metabolites that occur during HSC inactivation using low-concentration sorafenib.</p><p><strong>Methods: </strong>Human HSCs (LX-2) were activated by treatment with transforming growth factor (TGF)-β to create a fibrotic environment. The activated cells were treated with sorafenib and then subjected to transcriptomic and lipidomic analyses. In the transcriptomic analysis, statistical significance was assessed using adjusted P-values based on the Benjamini-Hochberg method, whereas significance in the lipidomic analysis was evaluated using MetaboAnalyst.</p><p><strong>Results: </strong>During fibrogenesis, we observed upregulation of extracellular matrix-related genes (COL1A1 (P < .001), FN1 (P < .001), THBS1 (P < .001), P4HA3 (P < .01)) and CXCL12 (P < .01), which is an upstream regulator of the Raf/MEK/ERK and PI3K/AKT signaling pathways. Meanwhile, dihydroceramide (dhCer) and dihydrosphingomyelin (dhSM) levels decreased (both P < .001). In contrast, sorafenib-induced antifibrotic conditions significantly reversed these molecular and lipidomic trends (all P < .01).</p><p><strong>Conclusions: </strong>In light of the observed trends, we propose that activating the dhSM synthesis pathway may play a regulatory role in fibrosis. Collectively, our study provides novel lipid-based insights into the molecular mechanisms underlying antifibrotic responses.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153785"},"PeriodicalIF":2.2,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832989","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":"Serpinh1 promotes fracture healing by enhancing osteogenesis via activation of the Wnt/β-catenin signaling pathway.","authors":"Zhehui Tu, Chenchen Xu, Yuanxin Zhu, Yiqiang Li Li, Hongwen Xu","doi":"10.1016/j.bbrc.2026.153864","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153864","url":null,"abstract":"<p><strong>Background: </strong>The process of fracture healing encompasses tightly regulated cellular and molecular interactions. However, the precise regulatory mechanisms that orchestrate osteogenesis during bone regeneration remain unclear.</p><p><strong>Methods: </strong>Fracture healing-related key genes were identified by integrating transcriptomic datasets (GSE157460 and GSE152677) with four machine learning algorithms. Gain- and loss-of-function experiments were performed by inducing serine (or cysteine) peptidase inhibitor, clade H, member 1 (Serpinh1) overexpression in murine fracture sites and mouse bone marrow mesenchymal stem cells (mBMSCs), and by siRNA-mediated Serpinh1 knockdown in mBMSCs. Hematoxylin and eosin staining, Masson's trichrome staining, Western blot, quantitative real-time PCR, Alizarin Red S staining, alkaline phosphatase activity assay, and TOP/FOP luciferase reporter assay, were used to evaluate callus formation, osteogenic differentiation, and extracellular matrix remodeling.</p><p><strong>Results: </strong>Four key genes, including biglycan (Bgn), collagen, type XI, alpha 1(Col11a1), collagen, type V, alpha 1 (Col5a1), and Serpinh1 were upregulated in the mouse model of fracture healing. In the murine fracture model, Serpinh1 overexpression promoted fracture healing, collagen deposition, and osteogenic marker expression. In mBMSCs, Serpinh1 overexpression enhanced the expression of osteogenesis-related proteins, increased mineralized nodule formation, and elevated alkaline phosphatase staining and activity, whereas Serpinh1 knockdown exerted the opposite effects. Mechanistically, Serpinh1 activated the Wnt/β-catenin pathway, and its pro-osteogenic effects were markedly abolished by methyl 3-[(4-methylphenyl)sulfonyl]amino-benzoate, a specific inhibitor of β-catenin.</p><p><strong>Conclusion: </strong>Serpinh1 promotes fracture healing by enhancing osteogenic differentiation via Wnt/β-catenin signaling, suggesting that it may serve as a potential therapeutic target.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153864"},"PeriodicalIF":2.2,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855642","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":"A mechanistic framework for oxaliplatin-induced peripheral neuropathy: from neuronal vulnerability to neurotoxic persistence.","authors":"Bingyao Li, Zhijie Song, Mei Zhang, Ruoyi Zhang, Qimeng Xin, Wenlan Zhang, Ming Li","doi":"10.1016/j.bbrc.2026.153849","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153849","url":null,"abstract":"<p><p>Oxaliplatin-induced peripheral neuropathy (OIPN) is a common and dose-limiting adverse effect of oxaliplatin-based chemotherapy that markedly impairs treatment adherence and long-term quality of life. Despite extensive investigation, effective preventive and therapeutic strategies remain limited, reflecting the complex and multifactorial nature of its pathogenesis. In this review, we revisit the mechanisms underlying OIPN and propose an integrated, stage-dependent mechanistic perspective. Current evidence indicates that OIPN arises from dynamic interactions among multiple pathological processes operating across temporal and anatomical scales. Early oxaliplatin-induced neurotoxicity is primarily expressed as functional and electrophysiological disturbances, which manifest clinically as acute sensory symptoms such as cold hypersensitivity. With sustained exposure, these alterations progressively engage downstream neuroinflammatory and metabolic cascades, ultimately contributing to structural pathology, including axonal degeneration, and to chronic, often persistent, peripheral neuropathy. Importantly, these mechanisms form self-amplifying loops that facilitate the transition from reversible acute symptoms to irreversible structural damage, providing a mechanistic explanation for the limited success of single-target neuroprotective strategies. Emerging complementary mechanisms are briefly discussed to outline future research directions. By reorganizing current evidence into a hierarchical, stage-linked framework that connects upstream neuronal vulnerability, early functional dysfunction, and downstream inflammatory-structural persistence, this review aims to clarify not only the pathophysiological complexity of OIPN but also its implications for stage-specific and combination-based intervention strategies.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153849"},"PeriodicalIF":2.2,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832867","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":"AtGATA11 activates AtBCCP2 transcription in Arabidopsis in response to NaHCO₃ stress.","authors":"Yao Wang, Xiaoxue Ye, Min Wang, Fengfeng Li, Huifang Shen, Xinting Shen, Fei Wang, Rui Zhao, Zhebin Li, Ye Zhou, Rantian Liu, Bo Li, Shuwen Lu, Xinmiao Yao","doi":"10.1016/j.bbrc.2026.153844","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153844","url":null,"abstract":"<p><p>NaHCO₃-induced alkaline stress severely affects plant growth by imposing ionic, osmotic, and high-pH stress. However, the transcriptional mechanisms underlying plant responses to NaHCO₃ remain incompletely understood. In this study, RNA sequencing was performed to analyze transcriptomic changes in shoots and roots of wild-type Arabidopsis thaliana treated with 3 mM NaHCO₃ for 0, 4, 12, 24, and 48 h. Among the differentially expressed genes, AtBCCP2, encoding biotin carboxyl carrier protein 2, was identified as a NaHCO₃-responsive gene. Co-expression network analysis predicted several transcription factors potentially regulating AtBCCP2. Yeast one-hybrid and dual-luciferase assays demonstrated that the transcription factor AtGATA11 directly binds to the promoter of AtBCCP2 and activates its transcription. Notably, AtGATA11-mediated transcriptional activation of AtBCCP2 was significantly enhanced under NaHCO₃ treatment. These results identify AtGATA11 as a direct transcriptional regulator of AtBCCP2 during NaHCO₃ stress and provide molecular evidence for transcription factor mediated regulation in plant alkaline stress responses.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153844"},"PeriodicalIF":2.2,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832897","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":"40 Hz light flicker stimulation for neurodegenerative diseases: Mechanisms and clinical perspectives.","authors":"Ya Shu, Ze-Hua Ding, Xiao-Qian Chen, Feng Liu","doi":"10.1016/j.bbrc.2026.153858","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153858","url":null,"abstract":"<p><p>Neurodegenerative diseases are a class of disorders characterized by the progressive degeneration and dysfunction of neurons, such as Alzheimer's disease (AD) and Parkinson's disease (PD). Due to their high incidence rate, irreversible pathological processes and huge social and economic burdens, these diseases have become a major challenge in global public health. Light Flicker Stimulation (LFS), as a non-invasive form of physical therapy, shows significant neuroprotective potential by modulating electrical brain oscillations and particular signaling pathways. We critically examine the role of stimulation parameters (frequency, wavelength, multisensory combination) and discuss the state of clinical translation, including completed and ongoing trials, safety considerations, and technological innovations such as alternating bilateral stimulation and organic light-emitting diode (OLED) devices. By integrating mechanistic insights with clinical perspectives, this review aims to identify key gaps and future directions for harnessing 40 Hz LFS as a viable treatment for neurodegenerative diseases.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153858"},"PeriodicalIF":2.2,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832920","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":"CREST regulates the Ca²⁺ signaling-mediated circadian transcriptional rhythms of the Per1 and Dbp promoters by coactivating with CLOCK/BMAL1.","authors":"Daiki Miura, Takuzo Shimo, Yoshikazu Morishita, Takanobu Nakazawa, Satoshi Kida","doi":"10.1016/j.bbrc.2026.153859","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153859","url":null,"abstract":"<p><p>Circadian rhythms are generated by the periodic transcriptional regulation of a group of clock genes by the transcription factors clock circadian regulator (CLOCK) and basic helix-loop-helix ARNT-like 1 (BMAL1). Intracellular circadian rhythms are regulated by multiple signaling pathways. The calcium signaling pathway especially plays an important role in the rhythmic regulation of clock genes; however, the precise molecular mechanisms underlying calcium signaling-mediated rhythmic transcriptional regulation remain largely unclear. Here, we found that calcium-responsive transactivator (CREST) plays an important role in activating period circadian regulator 1 (Per1) and D-box binding PAR bZIP transcription factor (Dbp) gene expression by increasing intracellular calcium ion concentrations and rhythmic transcriptional regulation of these genes. Importantly, CREST increases the promoter activity of Per1 and Dbp by forming a complex with CLOCK and BMAL1. Finally, we found that CREST binds to the E-box-containing promoters of Per1 and Dbp. Taken together, we conclude that the formation of CREST and CLOCK/BMAL1 complexes at the E-boxes of the Per1 and Dbp promoters increases their mRNA expression in response to increased intracellular calcium ion concentrations.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153859"},"PeriodicalIF":2.2,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832976","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":"Antiproliferative effects of TUBB3 in ERα-positive postmenopausal breast cancer model cells.","authors":"Masayo Hirao-Suzuki, Koki Kanameda, Shuso Takeda","doi":"10.1016/j.bbrc.2026.153836","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.153836","url":null,"abstract":"<p><p>Long-term estrogen-deprived (LTED) cells were obtained from parental MCF-7 breast cancer (BC) cells cultured under conditions of prolonged estrogen deprivation. In LTED cells, which mimic estrogen receptor α (ERα)-positive BC that has relapsed after endocrine therapy, βIII-tubulin (TUBB3) expression is downregulated. However, the biological significance of TUBB3 downregulation is unclear. To address this, we assessed the effects of siRNAs targeting individual TUBB isotypes. Among of them, only TUBB3-targeting siRNA stimulated the proliferation of MCF-7 cells, but it did not affect LTED cells. After treating LTED cells with 17β-estradiol (E2), the upregulation of TUBB3 expression and antiproliferative effects were detected, suggesting that TUBB3 mediates the antiproliferative effects of E2. Furthermore, the attenuated TUBB3 expression was related to poor prognosis in patients with ERα-positive BC receiving endocrine therapy. These findings identify TUBB3 as an E2-sensitive antiproliferative molecule in ERα-positive BC cells, suggesting that it could be targeted for endocrine therapy-resistant BC.</p>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"821 ","pages":"153836"},"PeriodicalIF":2.2,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810269","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}