{"title":"Expression of concern for \"Influence of maternal lipid profile on placental protein expression of LDLr and SR-BI\" [Biochem. Biophys. Res. Commun. 359 (2007), 8-14, 10.1016/j.bbrc.2007.05.002].","authors":"","doi":"10.1016/j.bbrc.2026.154708","DOIUrl":"10.1016/j.bbrc.2026.154708","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154708"},"PeriodicalIF":2.5,"publicationDate":"2026-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135026","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":"Expression of concern for \"Two membrane juxtaposed signaling modules in ANF-RGC are interlocked\" [Biochem. Biophys. Res. Commun. 332, (2005), 149-156, 10.1016/j.bbrc.2005.04.102].","authors":"","doi":"10.1016/j.bbrc.2026.154707","DOIUrl":"10.1016/j.bbrc.2026.154707","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154707"},"PeriodicalIF":2.5,"publicationDate":"2026-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126562","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":"Expression of Concern to \"Mesenchymal stem cell-derived extracellular vesicles alone or in conjunction with a SDKP-conjugated self-assembling peptide improve a rat model of myocardial infarction\" [Biochem. Biophys. Res. Commun. 524, (2020), 903-909].","authors":"","doi":"10.1016/j.bbrc.2026.154652","DOIUrl":"10.1016/j.bbrc.2026.154652","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154652"},"PeriodicalIF":2.5,"publicationDate":"2026-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079517","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":"Expression of Concern to \"MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R\" [Biochem. Biophys. Res. Commun. 453 (2014) 728].","authors":"","doi":"10.1016/j.bbrc.2026.154651","DOIUrl":"10.1016/j.bbrc.2026.154651","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154651"},"PeriodicalIF":2.5,"publicationDate":"2026-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079508","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 \"Regulation and functional role of eEF1A2 in pancreatic carcinoma\" [Biochem. Biophys. Res. Commun. 380, (2009), 11-16].","authors":"Haixia Cao, Qi Zhu, Jia Huang, Baiwen Li, Su Zhang, Weiyan Yao, Yongping Zhang","doi":"10.1016/j.bbrc.2026.154716","DOIUrl":"https://doi.org/10.1016/j.bbrc.2026.154716","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":" ","pages":"154716"},"PeriodicalIF":2.5,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179311","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":"Cytoophidia: Implications and opportunities for cancer treatment","authors":"Zelin Pan , Kaili Deng , Zhe Sun","doi":"10.1016/j.bbrc.2026.153504","DOIUrl":"10.1016/j.bbrc.2026.153504","url":null,"abstract":"<div><div>Cytidine triphosphate synthase (CTPS), the rate-limiting enzyme in de novo CTP synthesis, forms filamentous structures known as cytoophidia, which are evolutionarily conserved across species and cell types. These dynamic structures are regulated by cellular metabolic states, stress, and post-translational modifications. Cytoophidia are believed to play a vital role in regulating nucleotide biosynthesis, ensuring cellular homeostasis, and responding to metabolic stress through the modulation of CTPS activity. In cancer cells, where the demand for nucleotides is heightened, cytoophidia may be essential for supporting proliferation and survival. This review delves into the growing understanding of cytoophidia, highlighting their significance in cancer biology and potential as therapeutic targets. Understanding how cytoophidia regulate the balance between CTPS stabilization and degradation could provide valuable insights into cancer metabolism, offering novel therapeutic opportunities. Targeting the mechanisms that govern cytoophidia formation presents a potential strategy for cancer therapy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153504"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147316184","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}
Huiyi Wang , Jing Wu , Zhendong Huang , Zhengkun Yang , Jiayi Ding , Xiaoxuan Wang , Zhengguo Cao
{"title":"Hyperparathyroidism drives periodontitis progression via parathyroid hormone-induced endoplasmic reticulum stress","authors":"Huiyi Wang , Jing Wu , Zhendong Huang , Zhengkun Yang , Jiayi Ding , Xiaoxuan Wang , Zhengguo Cao","doi":"10.1016/j.bbrc.2026.153512","DOIUrl":"10.1016/j.bbrc.2026.153512","url":null,"abstract":"<div><h3>Aims</h3><div>Given the high prevalence of periodontitis and potential for undetected primary hyperparathyroidism (pHPT) to exacerbate periodontal damage, managing pHPT in advanced periodontitis (stages III/IV) is critical. The causal link between pHPT and periodontitis remains unclear. This study aims to investigate the causal effect and mechanisms between hyperparathyroidism and periodontitis.</div></div><div><h3>Methods</h3><div>A two-sample Mendelian randomization study used genome-wide association studies (GWAS) summary data to explore the causal link between hyperparathyroidism and periodontitis, employing single nucleotide polymorphisms (SNPs) as instrumental variables and methods like MR-Egger regression and Weighted median for robust results. PTH levels were detected on samples from both healthy and periodontitis-affected gingival tissues and gingival crevicular fluids. We assessed the impact of PTH on periodontal inflammation through treating gingival fibroblasts with PTH and detecting endoplasmic reticulum stress-related markers. Transcriptomics and metabolomics analyses were integrated to explore genetic pathways related to PTH.</div></div><div><h3>Results</h3><div>Hyperparathyroidism increased the risk of periodontitis, but analyses of periodontitis on hyperparathyroidism showed no reverse causality. PTH levels increased in gingival tissues and gingival crevicular fluid. Multi-omics analysis revealed significant gene and metabolite enrichment in calcium signaling and parathyroid hormone pathways. Since calcium ions are mainly from the endoplasmic reticulum, we focused on endoplasmic reticulum stress and found its effect on lessening PTH-induced periodontal inflammation.</div></div><div><h3>Conclusions</h3><div>This study suggests that periodontitis may serve as a warning sign for pHPT, highlighting the importance of screening for hyperparathyroidism in periodontitis patients. The principal molecules involved in the endoplasmic reticulum stress pathway present promising therapeutic targets for improving periodontal health in patients with hyperparathyroidism.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153512"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343500","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}
Nada H. Hussein , Mahadi Hasan , Renata Akhmetzianova , Hai Yu , Susumu Kohno , Takiko Daikoku , Akira Orimo , Chiaki Takahashi
{"title":"RECK attenuates CAF-mediated promotion of epithelial-mesenchymal transition in breast cancer","authors":"Nada H. Hussein , Mahadi Hasan , Renata Akhmetzianova , Hai Yu , Susumu Kohno , Takiko Daikoku , Akira Orimo , Chiaki Takahashi","doi":"10.1016/j.bbrc.2026.153498","DOIUrl":"10.1016/j.bbrc.2026.153498","url":null,"abstract":"<div><div>Cancer associated fibroblasts (CAFs) play pivotal roles in modulating behaviors of tumor cells through various mechanisms. Here we analyzed a pair of fibroblastic cells derived from stromal tissue of breast cancer (BC-CAFs) or corresponding normal mammary microenvironment (NMFs). We found that the reversion-inducing cysteine-rich protein with Kazal motif (RECK) was highly expressed only in NMFs. Conditioned media derived from BC-CAFs enhanced epithelial-mesenchymal transition (EMT) in breast cancer cells significantly stronger than NMFs. Similarly, BC-CAFs induced EMT in co-injected breast cancer cells when xenografted into immune-compromised mice. These activities of BC-CAFs were significantly suppressed by RECK overexpression. BC-CAFs exhibited higher rate of active/latent TGF-β1 and active/pro-MMP-2. Induction of RECK in BC-CAFs significantly antagonized EMT induction with diminished activation of TGF-β1 and pro-MMP-2. Inversely, depletion of RECK in NMFs promoted EMT with enhancement of TGF-β1 and pro-MMP2 activation. BC-CAFs express higher level of histone deacetylase 1/2 (HDAC-1/2). Multiple HDAC inhibitors induced RECK in BC-CAFs with concomitant decrease in TGF-β 1and pro-MMP2 activation and ability to induce EMT. BC-CAFs exhibited higher histone acetylation in the promoter of RECK. These findings suggest that RECK ectopic expression in BC-CAFs suppresses TGF-β1 maturation by inhibiting pro-MMP-2 activation thereby attenuates EMT and that RECK promoter deacetylation occurs in fibroblasts associated with developing breast cancer. HDAC inhibitors may exhibit therapeutic efficacy in breast cancer by inducing RECK in BC-CAFs.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153498"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147347132","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}
Roman Dekhtiarenko , Katarina Polcicova , Zuzana Sevcikova Tomaskova
{"title":"Translocator protein in touch with mitochondrial chloride intracellular channel CLIC5","authors":"Roman Dekhtiarenko , Katarina Polcicova , Zuzana Sevcikova Tomaskova","doi":"10.1016/j.bbrc.2026.153537","DOIUrl":"10.1016/j.bbrc.2026.153537","url":null,"abstract":"<div><div>Cardiac arrhythmias rank among the leading causes of death worldwide. They frequently develop during ischemia/reperfusion, when fluctuations in oxygen and nutrient supply occur. Reperfusion can elevate levels of oxygen radicals, and both metabolic and oxidative stress have been shown to trigger arrhythmias by inducing cyclic changes in mitochondrial membrane potential. These fluctuations are mediated by chloride channels believed to correspond to the CLIC5 isoform of intracellular chloride channels. The cardioprotective effects have been observed following administration of 4-chlorodiazepam (4Cl-DZP), a specific ligand of the mitochondrial translocator protein TSPO, as well as after treatment with a non-specific anion channel inhibitor. Although 4Cl-DZP is thought to influence chloride channel activity indirectly through TSPO, the details of this interaction remain unclear. CLIC5 has been localized to the inner mitochondrial membrane. Based on the comparison of single-channel properties, it may represent a candidate for the molecular identity of the centum-pS channel. The potential physical association between CLIC5 and TSPO was investigated. To assess the spatial proximity of CLIC5 and TSPO, we performed Förster resonance energy transfer (FRET) measurements in immunolabeled cardiomyoblasts using acceptor photobleaching configuration. The observed FRET efficiency between CLIC5 and TSPO was 24%, comparable to the 28% efficiency measured in the positive control and substantially higher than the 7% efficiency observed in the negative control. These findings support the hypothesis that, if CLIC5 indeed constitutes the centum-pS channel, TSPO is positioned in sufficiently close proximity to modulate its activity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"810 ","pages":"Article 153537"},"PeriodicalIF":2.2,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324084","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}