Biochemical and biophysical research communications最新文献

{"title":"A novel prohibitin inhibitor acts as a dual inhibitor of angiogenesis and fibrosis","authors":"Ken'ichiro Hayashi ,&nbsp;Masaaki Kobayashi ,&nbsp;Kotaro Mori ,&nbsp;Yoshiaki Nakagawa ,&nbsp;Bunta Watanabe ,&nbsp;Takahiro Masuya ,&nbsp;Atsushige Ashimori ,&nbsp;Fumiaki Higashijima ,&nbsp;Takuya Yoshimoto ,&nbsp;Tsuyoshi Morita ,&nbsp;Toshiyuki Murai ,&nbsp;Saki Kirihara-Kojima ,&nbsp;Kazuhiro Kimura","doi":"10.1016/j.bbrc.2026.153386","DOIUrl":"10.1016/j.bbrc.2026.153386","url":null,"abstract":"<div><div>We previously showed that the benzoylphenylurea derivative BPU17 inhibits epithelial-mesenchymal transition and acts as an antifibrotic agent. This compound acts as a prohibitin (PHB) inhibitor by directly binding to PHB1. This binding disrupts the interaction between PHB1 and PHB2, leading to mild mitochondrial dysfunction. Here, we investigated the effect of BPU17 on angiogenesis using primary cultures of human vascular and microvascular endothelial cells, as well as a mouse model of choroidal neovascularization (CNV). A series of studies has shown that BPU17 inhibits angiogenesis both in vitro and in vivo. The molecular mechanism is that BPU17 inhibits serum response factor (SRF)/CArG box-mediated transcription by repressing the expression of SRF and its cofactor myocardin-related transcription factors (MRTF-A and -B [MRTF]). This defect causes the downregulation of adaptor and cell adhesion molecules such as vinculin and integrins, leading to the inhibition of angiogenesis. This inhibitory effect is closely associated with mild mitochondrial dysfunction, and siRNA-mediated knockdown of PHB1 similarly inhibits angiogenesis. Given that age-related inflammatory responses and subsequent choroidal neovascularization (CNV) contribute to the development of neovascular age-related macular degeneration (nAMD), this novel PHB inhibitor holds promise as a treatment for nAMD through its dual inhibitory effects on angiogenesis and fibrosis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153386"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112169","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":"Crystal structure and functional characterization of the microalgal carotenoprotein AstaP-pink1","authors":"Yury B. Slonimskiy ,&nbsp;Daria A. Lunegova ,&nbsp;Andrey S. Nikolaev ,&nbsp;Ilya O. Matyuta ,&nbsp;Konstantin E. Klementiev ,&nbsp;Vladimir O. Popov ,&nbsp;Konstantin M. Boyko ,&nbsp;Ivan Yu. Gushchin ,&nbsp;Nikolai N. Sluchanko","doi":"10.1016/j.bbrc.2026.153374","DOIUrl":"10.1016/j.bbrc.2026.153374","url":null,"abstract":"<div><div>The recently discovered family of microalgal water-soluble astaxanthin-binding proteins (AstaPs) functions in carotenoid sequestration and transfer. We present the crystal structure and characterization of AstaP-pink1, a homolog from <em>Scenedesmus</em> sp. We show that despite low sequence identity with the known AstaP-orange1, AstaP-pink1 also binds various xanthophylls, but in contrast to AstaP-orange1, induces a pronounced bathochromic shift and a near-UV spectral bump upon binding ketocarotenoids, which is reminiscent of photoactivated Orange Carotenoid Protein (OCP). Mutagenesis and domain-swap experiments indicate that its unique spectral tuning likely results from carotenoid isomerization, forced by the interplay between its N-terminal jaw and body subdomains connected by the hinge loop of different sequence and length. This study attempts to rationalize the spectral and functional diversification of AstaPs and highlights their potential as engineered modules for carotenoid delivery.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153374"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117460","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":"Establishment of immortalized murine cardiac fibroblasts for visualizing cytosolic ATP dynamics with a genetically encoded optical indicator","authors":"Ariunbold Chuluun-Erdene ,&nbsp;Takahiro Kuchimaru ,&nbsp;Takayuki Isagawa ,&nbsp;Tatsuyuki Sato ,&nbsp;Hiroki Sugimoto ,&nbsp;Kazutoshi Ono ,&nbsp;Daigo Sawaki ,&nbsp;Shigeru Sato ,&nbsp;Masamichi Yamamoto ,&nbsp;Norihiko Takeda","doi":"10.1016/j.bbrc.2026.153377","DOIUrl":"10.1016/j.bbrc.2026.153377","url":null,"abstract":"<div><div>Cardiac fibroblasts (CFs) are the predominant non-myocyte cell type in the heart and play central roles in extracellular matrix remodeling and intercellular signaling during cardiac physiology and pathology. However, the bioenergetic basis underlying CF functions remains poorly understood, mainly due to the lack of tools for visualizing intracellular adenosine triphosphate (ATP) dynamics with high spatiotemporal resolution. Here, we established immortalized murine cardiac fibroblasts stably expressing the genetically encoded ATP indicator GO-ATeam2 based on Förster Resonance Energy Transfer (FRET). The resulting CF7/GO-ATeam2 cell line allows real-time and quantitative monitoring of cytosolic ATP levels in living cells. CF7/GO-ATeam2 cells exhibited robust proliferation and quick responses to change of cytosolic ATP level. We demonstrated dynamic cytosolic ATP imaging upon pharmacological perturbations of oxidative phosphorylation and glycolysis, as well as under growth factor stimulation. Our work provides the CF7/GO-ATeam2 platform, a versatile cellular resource for dissecting the metabolic regulation of cardiac fibroblasts, offering new opportunities to explore energy dynamics in cardiac physiology and disease.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153377"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123473","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":"Biological effectiveness of superficial X-ray in mammalian cells through precise dosimetry and Monte Carlo simulations","authors":"Reham Barghash ,&nbsp;Piyawan Chailapakul ,&nbsp;Amber R. Prebble ,&nbsp;Del Leary ,&nbsp;Takamitsu A. Kato","doi":"10.1016/j.bbrc.2026.153352","DOIUrl":"10.1016/j.bbrc.2026.153352","url":null,"abstract":"<div><div>This study evaluates the radiobiological effectiveness comparing superficial X-rays to Cs-137 in V79 and U2OS cells cultured in T25 flasks using colony formation assays. Additional dosimetric care was given to maintaining equal absolute dose for all beam qualities, correcting for absorption and scattering in the flask, and quantifiable interpretation due to dose of the spatial differences in cell survival with significantly higher survival near the flask's edges. Ion chamber measurements quantified flask lid attenuation (6.9 %, 2.4 %, and 1.9 % for 50, 70, and 100 kVp), enabling dose correction for accurate survival analysis. CT-based Monte Carlo simulations revealed thicker flask walls and the meniscus effect created a 35 % dose reduction from flask center to edges, directly explaining the observed survival patterns. Monte Carlo simulation also predicted an increased secondary electron production at higher energies. These results emphasize the necessity of precise dosimetry in low-energy X-ray studies. Combined experimental and computational approaches enhanced reliability of radiobiological assessments. Survival curves yielded Relative Biological Effectiveness (RBE) values for 50 kVp X-ray of 1.45 (V79) and 1.64 (U2OS); 1.41 (V79) and 1.55 (U2OS) at 70 kVp; and 1.23 (V79) and 1.36 (U2OS) at 100 kVp, relative to Cs-137.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153352"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123494","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":"Cetylpyridinium chloride inhibits the polarization of tumor-associated macrophages and the proliferation of triple-negative breast cancer cells","authors":"Gaoyue Jiang ,&nbsp;Chunxia Li ,&nbsp;Baihui Jia ,&nbsp;Meng Lu ,&nbsp;Yuqing Lei ,&nbsp;Kefeng Lu ,&nbsp;Tao cui ,&nbsp;Huihui Li","doi":"10.1016/j.bbrc.2026.153389","DOIUrl":"10.1016/j.bbrc.2026.153389","url":null,"abstract":"<div><h3>Objectives</h3><div>Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Due to its radiotherapy resistance, high metastasis rate and recurrence rate, the prognosis is poor. So far, effective therapeutic drugs for it remain elusive. Cetylpyridinium chloride (CPC) has initially demonstrated anti-tumor properties in various tumors. Therefore, the aim of this study is to explore the intervention effect of CPC on macrophages in the tumor microenvironment (TME) and its therapeutic effect on TNBC.</div></div><div><h3>Methods</h3><div>The effects of CPC on macrophage polarization and expression changes were evaluated by WB and RT-qPCR. Multiple TNBC cell lines and non-cancer cells were exposed to CPC under different conditions (concentration and duration), and cell survival and proliferation were assessed by CCK8 and colony formation. The effects of CPC on apoptosis, migration and invasion of TNBC cells were further evaluated. The mitochondrial status was assessed by Mito-Tracker Red CMXRos staining, mitochondrial protein expression detection and ATP content detection to explain the cause of apoptosis. The effect of CPC on TNBC growth was further confirmed in animal models.</div></div><div><h3>Results</h3><div>Our results demonstrated that CPC (2 μM) inhibited the M2 polarization of macrophages induced by interleukin-4 (IL-4) and tumor secretions, and reduced their characteristic secretions that promote tumor growth. Meanwhile, CPC significantly suppressed the proliferation of multiple TNBC cell lines, induced mitochondrial damage, significantly decreased cellular ATP levels, and ultimately led to tumor cell apoptosis. Moreover, TNBC cells are more sensitive to CPC than non-tumor cells. Additionally, CPC significantly inhibited the migration and invasion of TNBC cells. Finally, we confirmed the growth inhibitory effect of CPC on TNBC in vivo.</div></div><div><h3>Conclusion</h3><div>CPC has dual effects: it inhibits the M2 polarization of tumor-associated macrophages (TAMs) and directly suppresses the proliferation and invasion of TNBC cells, ultimately effectively inhibiting the growth of TNBC in vivo. Considering that CPC has been administered in humans as a safe drug-disinfectant for decades, our study here provides a molecular basis for the application of CPC as a potential option to clinical treatments of TNBC.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153389"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137069","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":"KLHL20 alleviates high glucose-induced mitochondrial apoptosis in renal tubular cells by targeting DAPK1 for ubiquitination and degradation","authors":"Yi Lei ,&nbsp;Chenlin Gao ,&nbsp;Xin Zhao ,&nbsp;Betty Yuen Kwan Law ,&nbsp;Yong Xu","doi":"10.1016/j.bbrc.2026.153345","DOIUrl":"10.1016/j.bbrc.2026.153345","url":null,"abstract":"<div><div>Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease, driven by hyperglycemia-induced mitochondrial apoptosis in renal tubular epithelial cells. Death-associated protein kinase 1 (DAPK1) is a key mediator of cell death, but its regulation in DKD remains unclear. Here, we investigated the mechanisms underlying DAPK1 upregulation and its role in mitochondrial apoptosis under high glucose (HG) conditions in HK-2 cells and <em>db/db</em> mouse models. In <em>db/db</em> mice, renal DAPK1 protein levels were elevated, while KLHL20 levels were reduced, correlating with glomerular and tubular injury. In HK-2 cells, HG (33 mM, 48 h) significantly increased DAPK1 mRNA and protein levels while prolonging its half-life. Mechanistically, HG transcriptionally suppressed KLHL20, an E3 ubiquitin ligase adaptor that targets DAPK1 for proteasomal degradation. Co-immunoprecipitation confirmed KLHL20-DAPK1 interaction and showed reduced DAPK1 ubiquitination under HG. Overexpression of <em>KLHL20</em> restored DAPK1 ubiquitination and reduced its protein levels without affecting mRNA, confirming post-translational regulation. Functionally, <em>DAPK1</em> knockdown attenuated HG-induced mitochondrial apoptosis. <em>KLHL20</em> overexpression similarly protected against HG-induced apoptosis, but this effect was abrogated by <em>DAPK1</em> co-overexpression, establishing DAPK1 as a critical downstream effector. These findings reveal a novel KLHL20-DAPK1 axis where HG stabilizes DAPK1 by downregulating KLHL20, promoting mitochondrial apoptosis in renal tubular cells. Targeting this pathway may offer therapeutic strategies for DKD.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153345"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117575","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":"Nanoemulsion in cancer therapy: Enhancing the therapeutic efficacy of capecitabine and 5-fluorouracil in colorectal cancer with thymoquinone nanoemulsion","authors":"Sama Torkashvand ,&nbsp;Sohrab Kazemi ,&nbsp;Ali Akbar Moghadamnia","doi":"10.1016/j.bbrc.2026.153331","DOIUrl":"10.1016/j.bbrc.2026.153331","url":null,"abstract":"<div><div>Chemotherapy is a significant treatment for cancer; however, it is frequently associated with deleterious side effects. Thymoquinone (TQ), a naturally occurring compound, has been reported to exhibit notable anti-cancer potential. The present study focuses on the <em>in vitro</em> effects of TQ-loaded nanoemulsion (TQ-NE) as an independent treatment and alongside the prevalent chemotherapeutic agents, 5-fluorouracil (5-FU) and capecitabine (CAP), on a colorectal cancer (HT-29) cell line. A TQ-NE formulation was synthesized and characterized, revealing an average particle size of 129.5 nm. The IC₅₀ values for CAP, 5-FU, TQ, NE (carrier), and TQ-NE were 39.57, 61.01, 21.81, 218.4, and 15.12 μM, respectively. Cytotoxic effects were examined in both HT-29 cells and fibroblasts, revealing that TQ-NE enhanced the sensitivity of cancer cells to chemotherapeutic agents. When combined with 5-FU or CAP, TQ-NE produced a greater reduction in cell viability than TQ alone, indicating synergistic interaction. Flow cytometry analysis further revealed that TQ-NE induced distinct apoptotic responses compared to the control, whereas its combination with chemotherapy drugs showed a different pattern.</div><div>These findings suggest that TQ-NE can enhance the cytotoxic activities of 5-FU and CAP <em>in vitro</em>. Furthermore, using lower concentrations of TQ-NE could potentiate the inhibitory effects of 5-FU and CAP, presenting a promising strategy for improving colorectal cancer (CRC) treatment outcomes while potentially reducing the adverse effects related to higher doses of conventional chemotherapy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153331"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123538","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":"Spatial organization of ER-derived protein aggregates in the nucleus requires the Hsp70-family member BiP","authors":"Shoukang Du ,&nbsp;Yuhan Wang ,&nbsp;Ting Gang Chew","doi":"10.1016/j.bbrc.2026.153406","DOIUrl":"10.1016/j.bbrc.2026.153406","url":null,"abstract":"<div><div>Cells maintain proteostasis by sequestering misfolded proteins into deposition sites. Aggregation-prone endoplasmic reticulum (ER) proteins form membrane-bound nuclear compartments that are cleared during cell division, yet the mechanisms underlying their spatial organization remain unclear. Here, using transcriptomic and proteomic analyses, we identified the ER-localized Hsp70 chaperone BiP as a key player. Genetic depletion or chemical inhibition of BiP prevented nuclear aggregate formation, while manipulating BiP regulators perturbed the aggregate formation. BiP-driven aggregation precedes the inner nuclear membrane synthesis that encapsulated the aggregates. Under proteostatic stress, nuclear aggregates localized adjacent to ER-derived aggregates. Our findings demonstrate that BiP is essential for organizing ER-derived aggregates in the nucleus, which further regulate nuclear proteostasis through spatial interactions with nuclear aggregates.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153406"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131150","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":"Proline metabolism supports the hepatocellular carcinoma cell survival by mitigating ROS generation under nutrient starvation","authors":"Jinglian Mo ,&nbsp;Ziming Liu ,&nbsp;Jialin Fu ,&nbsp;Qichao Ge ,&nbsp;Yiying Qu ,&nbsp;Nan Ge ,&nbsp;Yang Liu","doi":"10.1016/j.bbrc.2026.153392","DOIUrl":"10.1016/j.bbrc.2026.153392","url":null,"abstract":"<div><h3>Background</h3><div>Proline supplementation promotes proliferation and invasion in cancers under acute nutrient deprivation. However, its molecular basis in hepatocellular carcinoma is not fully understood yet. This study investigates how proline metabolism promotes hepatocellular carcinoma (HCC) cell proliferation and survival during nutrient starvation.</div></div><div><h3>Methods</h3><div>Proline metabolism-related protein expression in HCC versus paracarcinoma tissues was analyzed using The Cancer Genome Atlas database. HCC cell viability was quantified via Cell Counting Kit 8 assays, and colony formation capacity was evaluated. Intracellular ROS levels were measured by flow cytometry. Autophagic flux was assessed by GFP/mCherry fluorescence ratio and autophagy-related proteins by immunoblotting. Lipid droplet deposition was visualized using Hoechst 33342 and BODIPY 493/503 staining.</div></div><div><h3>Results</h3><div>Proline metabolism-related proteins were significantly upregulated in HCC tissues compared to paracarcinoma controls. Under acute nutrient stress, exogenous proline reduced cellular ROS levels, attenuated lipid droplet accumulation, and suppressed excessive autophagy in HCC cells. Proline rescued nutrient deprivation-induced tumor growth inhibition, which could be reversed by H₂O₂ and rapamycin.</div></div><div><h3>Conclusion</h3><div>Proline metabolism sustains HCC cell survival during nutrient restriction by reducing ROS accumulation, thereby inhibiting lipid droplet formation and autophagy.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153392"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131129","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":"CEACAM6-positive extracellular vesicles released during Helicobacter pylori infection promote gastric tumor aggression","authors":"Debashish Chakraborty ,&nbsp;Supriya Samal ,&nbsp;Smaran Banerjee ,&nbsp;Aranya Pal ,&nbsp;Indrajit Poirah ,&nbsp;Gautam Nath ,&nbsp;Asima Bhattacharyya","doi":"10.1016/j.bbrc.2026.153379","DOIUrl":"10.1016/j.bbrc.2026.153379","url":null,"abstract":"<div><div>Extracellular vesicles (EVs) are lipid bilayer-encased nano-size carriers that orchestrate molecular exchanges in the tumor microenvironment (TME) and carry significant information about the tumor development, progression and aggressiveness. Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) mediates <em>Helicobacter pylori</em> adhesion to gastric epithelial cells and is markedly upregulated in gastric cancer (GC). This study identified that EVs secreted by <em>H. pylori</em>-infected gastric cancer cells (GCCs) were loaded with CEACAM6. In order to examine the tumorigenic potential of EVs released by <em>H. pylori</em>-infected cells with and without <em>CEACAM6</em> overexpression, EVs were thoroughly characterised and several functional assays were conducted. <em>CEACAM6</em> overexpressed cell-derived EVs mimicked the elevated status of CEACAM6 as in their source cells which were found to be further enhanced in EVs collected from infected cells. As revealed by the population-doubling, clonogenicity, wound-healing and matrigel invasion assays, CEACAM6-enriched EVs promoted oncogenic properties of recipient cells while EVs from <em>H. pylori</em>-infected <em>CEACAM6</em>-expressing cells further amplified these tumorigenic abilities. A novel approach of EV-sonication and fractionation identified that CEACAM6 were mainly located in the EV membrane. Interestingly, aligned with the finding of elevated CEACAM6 protein in the <em>H. pylori</em> infection-led metastatic GC tissue samples, sera from those GC patients exhibited significantly high CEACAM6 compared to those from the healthy volunteers. Collectively, these findings highlight CEACAM6-containing EVs as mediators of tumorigenesis. This study also showcases the technical, translational and clinical advantages of considering CEACAM6 as a diagnostic biomarker for the detection of GC in a minimally-invasive manner.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"805 ","pages":"Article 153379"},"PeriodicalIF":2.2,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131162","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}