Nikhil Y. Gangadhara , Manju B , P Kiran Kumar , Honnur Krishna , Anantharaman Shivakumar , Ravishankar H. Sadashivanna , Avinash Krishnegowda
{"title":"Evaluation of peroxidase mimicking behaviour of V2O5 nanozymes with various morphologies and its application as glucose sensor via cascade mechanism in human serum samples","authors":"Nikhil Y. Gangadhara , Manju B , P Kiran Kumar , Honnur Krishna , Anantharaman Shivakumar , Ravishankar H. Sadashivanna , Avinash Krishnegowda","doi":"10.1016/j.bbrc.2025.151758","DOIUrl":"10.1016/j.bbrc.2025.151758","url":null,"abstract":"<div><div>A simple spectrophotometric method is presented for quantifying glucose and H<sub>2</sub>O<sub>2</sub> using <em>p</em>-aminophenol sulfate-(PAP) & N-(1-Naphthyl) ethylenediamine dihydrochloride-(NEDA) as novel chromogenic reagents with different morphological V<sub>2</sub>O<sub>5</sub> nanoparticles (NPs) as peroxidase mimicking nanozyme. For glucose, the method was linear in the range of 0.0289 and 0.925 mM for HRP and NPs. The substrate and nanozymes interaction was established using K<sub>m</sub> values, which were satisfactory. Recovery studies were performed with glucose and found between 83.98 % and 99.08 % for NPs and 88.48 to 99.35 for HRP. LOD range of 0.0194–0.0351 mM and LOQ range of 0.0588–0.1064 mM was observed with NPs, whereas for HRP, LOD was 0.02 and LOQ was 0.0607 mM. Maltose, sucrose, fructose, mannose, and galactose, considered potential interferants in glucose assay methods, provided negligible interference with the proposed method. Based on XRD data, the average crystalline size of the NPs was calculated using Scherrer's equation and Williamson-Hall plot and ranged between 29.14 and 45.42 nm, 32.5 and 45.7 nm, respectively. SEM and TEM images confirm the morphology of V<sub>2</sub>O<sub>5</sub> Nps were vanadium nanosheets (VNShs), nanoflowers (VNFws), and nanospheres (VNSps). DLS data revealed the Zeta potential of NPs in the range −4.5mv to 4.6mv. XPS confirms the NPs are in the V<sub>2</sub>O<sub>5</sub> state.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"762 ","pages":"Article 151758"},"PeriodicalIF":2.5,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791742","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}
Souvik Das, Bhagath Kumar Palaka, Raju Kuiry, Swarup Roy Choudhury
{"title":"Insights into the interactions of RWP-RK and their targets: Role of serine and its conservation across species","authors":"Souvik Das, Bhagath Kumar Palaka, Raju Kuiry, Swarup Roy Choudhury","doi":"10.1016/j.bbrc.2025.151750","DOIUrl":"10.1016/j.bbrc.2025.151750","url":null,"abstract":"<div><div>The RWP-RK domain is a key DNA-binding domain found in all NIN (Nodule Inception)/NLP (NIN-like proteins) and RKD (RWP-RK Domain Containing) transcription factors (TFs). The RWP-RK domain in NINs/NLPs contains a highly evolutionarily conserved sequence, RWPSRK, while in RKDs, the fourth serine (S) amino acid is substituted with either tyrosine (Y) or histidine (H). To regulate autoregulation of nodulation, the RWP-RK domain of NIN TF binds to the promoter region of CLE peptides but not RKDs. Therefore, investigating the protein-DNA interaction from a structural perspective is essential to understand the evolutionary significance of the serine (S) residue of the RWP-RK domain. Herein, we have modelled both the wild type (WT) and the variant RWP-RK domains containing substitutions like glutamic acid (E), tyrosine (Y), and histidine (H) and docked them with the modelled pCLE13 <em>cis</em>-element. Our docking results revealed that a helix-turn-helix (HTH) motif of the RWP-RK domain interacts with pCLE13. The WT HTH-DNA complex exhibited the most negative binding free energy, indicating a strong interaction, particularly hydrogen bonds acting between them. Simulation analysis of WT and variant models provided deeper insights into protein-DNA binding dynamics. The hydrogen bond occupancy percentage indicated that the fourth serine (S) residue is vital for maintaining a significant percentage of hydrogen bonds with DNA. The variants substituting this conserved serine (S) residue displayed energetic frustration upon binding to DNA and lost correlation among their residues. Overall, it suggested that serine (S) residue of the RWP-RK domain of all NINs/NLPs is crucial for appropriate protein-DNA interaction, which might be required for their biological relevance.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"763 ","pages":"Article 151750"},"PeriodicalIF":2.5,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823910","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}
Gongke Zhao , Chunzheng Li , Wan Liu, Jianing Wu, Xianguang Yang
{"title":"Understanding the Molecular Mechanisms of SORBS2 in TNBC Lung Metastasis","authors":"Gongke Zhao , Chunzheng Li , Wan Liu, Jianing Wu, Xianguang Yang","doi":"10.1016/j.bbrc.2025.151762","DOIUrl":"10.1016/j.bbrc.2025.151762","url":null,"abstract":"<div><div>Metastasis is the leading cause of recurrence and mortality in triple-negative breast cancer (TNBC), an aggressive subtype that predominantly spreads to the lungs, brain, bones, and liver, with lung metastasis being particularly prevalent. Despite the clinical significance of TNBC metastasis, the molecular mechanisms that drive lung-specific metastasis remain poorly understood. RNA-binding proteins (RBPs) are crucial regulators of post-transcriptional gene expression and are frequently dysregulated in cancers. This study identifies SORBS2 as a critical RBP implicated in TNBC lung metastasis. Using RNA sequencing (RNA-seq) and LACE-seq, we demonstrate that SORBS2 regulates a specific set of genes through direct binding to coding sequences (CDS), introns, and 3’ untranslated regions (UTRs), and its binding targets are linked to various pathways, including a possible association with Wnt/β-catenin signaling, among others. Functional assays confirm that SORBS2 knockdown inhibits proliferation, migration, and invasion in TNBC cells. These findings highlight SORBS2 as a key regulator of TNBC lung metastasis, with a context-dependent role that promotes metastatic behavior in highly metastatic TNBC cells, providing potential avenues for novel therapeutic strategies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"762 ","pages":"Article 151762"},"PeriodicalIF":2.5,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785724","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}
Malik Suliman Mohamed , Raya Soltane , Eid Alatwi , Ahlam Alasiri , Nuha Almulla , Karim Abdelkader , Ahmed M. Sayed
{"title":"Niclosamide as a potential antivirulence agent disrupting quorum sensing in Pseudomonas aeruginosa: A molecular and in silico approach","authors":"Malik Suliman Mohamed , Raya Soltane , Eid Alatwi , Ahlam Alasiri , Nuha Almulla , Karim Abdelkader , Ahmed M. Sayed","doi":"10.1016/j.bbrc.2025.151742","DOIUrl":"10.1016/j.bbrc.2025.151742","url":null,"abstract":"<div><div><em>Pseudomonas aeruginosa</em> is a formidable pathogen linked to various challenging infections. Quorum sensing (QS) plays a pivotal role in regulating the virulence factors of <em>P. aeruginosa</em>. Targeting QS represents a promising strategy for mitigating <em>P. aeruginosa</em> virulence. This study explores the potential of niclosamide (NIC) as an antivirulence agent, emphasizing its effects on biofilm formation, pigment production, and its molecular interaction with the QS regulator, LasR. A comprehensive methodology was employed, encompassing in-silico, molecular, and in vitro analyses to assess the antivirulence properties of NIC. Sub-inhibitory concentrations of NIC (64 μg/ml) were evaluated for their capacity to inhibit biofilm formation and pigment production in <em>P. aeruginosa</em>. NIC resulted in a 45.4 % reduction in biofilm formation, a 48.8 % decrease in pyocyanin production, and a 41.3 % reduction in rhamnolipid production. Furthermore, NIC displayed a dose-dependent antagonistic effect on LasR, with an IC50 of 5.82 ± 0.17 μM, without any noted agonistic activity. Molecular modeling and molecular dynamics (MD) simulations indicated that NIC interacts with LasR, hindering its dimerization and destabilizing its structure. These findings were corroborated by sedimentation velocity experiments and thermal shift assays. NIC shows considerable promise as an antivirulence agent against <em>P. aeruginosa</em> by disrupting the LasR-mediated QS system. Through its interaction with LasR, NIC inhibits biofilm formation and diminishes the production of critical virulence factors, making <em>P. aeruginosa</em> less virulent and more vulnerable to conventional antibiotics and immune responses.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"762 ","pages":"Article 151742"},"PeriodicalIF":2.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785726","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":"MGAT3 and MGAT5 overexpression alters the protein cargo of extracellular vesicles released by metastatic melanoma cells","authors":"Magdalena Wilczak , Magdalena Surman , Urszula Jankowska , Bozena Skupien-Rabian , Małgorzata Przybyło","doi":"10.1016/j.bbrc.2025.151749","DOIUrl":"10.1016/j.bbrc.2025.151749","url":null,"abstract":"<div><div>Extracellular vesicles (EVs) are potential non-invasive diagnostic, prognostic and therapeutic tools. Additionally, they are important contributors to tumorigenesis. Glycosylation has been found to modulate the composition of the EV proteome. Increased amounts of β1,6-branched N-glycans, synthesized by N-acetylglucosaminyltransferase V (GnT-V), are most commonly observed in melanoma and are associated with decreased cell adhesion and increased metastasis. The opposite effect is caused by the addition of bisecting GlcNAc by N-acetylglucosaminyltransferase III (GnT-III). To date, the impact of these enzymes on EV cargo in melanoma remains unexplored. Flow cytometry was used to study the surface glycosylation of genetic variants of WM266-4 melanoma cells with induced overexpression of GnT-III or GnT-V encoding genes (<em>MGAT3</em> or <em>MGAT5</em>) and EVs released by these cells.</div><div>LC-MS/MS proteomics was applied to analyze the effect of altered glycosylation on the proteome of released EVs, followed by detailed bioinformatic analysis. Flow cytometry analysis revealed dynamic changes in the surface glycosylation of EVs derived from melanoma cells overexpressing <em>MGAT3</em> or <em>MGAT5</em>. Induced overexpression of <em>MGAT3</em> or <em>MGAT5</em> also caused significant changes in the proteome of EVs. The proteomic analysis identified a total of 1770 microvesicular and 704 exosomal proteins that play different roles in melanoma progression, including those with established diagnostic/prognostic potential and those closely associated with melanoma onset. Proteomic profiling of EVs derived from cells overexpressing <em>MGAT3</em> and <em>MGAT5</em> revealed functional changes in EV protein content driven by glycosylation modifications. The study presented a potential multifaced application of melanoma-derived EVs for diagnostic and prognostic purposes.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"762 ","pages":"Article 151749"},"PeriodicalIF":2.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785725","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":"Neuroprotective effect of Thymus vulgaris on paraquat induced Parkinson's disease","authors":"Naheed Akhter , Iqra Rafiq , Amer Jamil , Zunera Chauhdary , Anum Mustafa , Aqsa Nisar","doi":"10.1016/j.bbrc.2025.151740","DOIUrl":"10.1016/j.bbrc.2025.151740","url":null,"abstract":"<div><div>The dramatic surge of neurodegenerative disorders among elderly population underscore the pressing demand for development of optimal and evidence based noninvasive natural treatment strategies. Paraquat exposure in animal models used in scientific studies can cause a variety of clinical signs of Parkinson disease (PD). The health benefits of thyme include antioxidant, anti-inflammatory, pulmonary, and neurological benefits. Thyme and other herbal treatments are frequently used to treat a variety of conditions, including neurological issues. The primary factor in the etiology of neurodegeneration is oxidative stress. Conventional treatments are indicated to potentially have negative side effects. The primary phytochemicals of <em>Thymus vulgaris</em> (TV), which are responsible for its unique therapeutic property of neuro-protection, include hydrocarbon and phenolic compounds like thymol and carvacrol. The goal of the current investigation was to examine <em>T. vulgaris'</em> potential for neuroprotection while also ensuring its safety. Analyses of the plant's physicochemical and phytochemical composition were performed by liquid chromatographic analysis. Neuro-behavioral and biochemical parameters were evaluated to determine the impact of <em>T. vulgaris</em> in paraquat induced parkinsonian rodents model. The neurobehavioral tests include open field tests for movement and exploration, Y maze test and elevated plus maze test for natural behavior, memory, and anxiety, hole board tests for exploratory behavior, ladder climbing, foot printing, and wire hanging tests for estimating neuromuscular coordination. <em>T. vulgaris</em> treatment significantly improved neurobehavioral parameters dose-dependently, Biochemical analysis revealed that extract treatment mitigated the declined level of antioxidant enzymes. RT-PCR analysis showed that in paraquat treated group mRNA expression of IL-1α, IL-1β, Alpha-Synuclein, TNF-α, and IL-6 was upregulated markedly. However, <em>T. vulgaris</em> treatment dose dependently down-regulated the mRNA expression of these genes. The groundbreaking results of current study revealed that <em>T. vulgaris</em> restored the degenerative alterations, neuro-inflammation, and nerve loss in the brain structure, as evident by histopathological investigation. Particularly remarkable restoration in neuropsychological and biochemical markers emphasize the medicinal potential of <em>T. vulgaris</em> as a revolutionary treatment for neurodegenerative disorders, offering new hope for millions worldwide afflicted by these devastating conditions.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"761 ","pages":"Article 151740"},"PeriodicalIF":2.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783460","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":"Effect of resveratrol and quercetin on SFRP4 as a biomarker of diabesity: In silico and in vivo studies","authors":"Asim Rehman , Shazia Anwer Bukhari , Zunera Chauhdary , Naheed Akhter , Razia Noreen","doi":"10.1016/j.bbrc.2025.151748","DOIUrl":"10.1016/j.bbrc.2025.151748","url":null,"abstract":"<div><div>The concurrent presence of complex metabolic disorders such as obesity and diabetes within an individual is known as diabesity. Various organs are involved in metabolic chronic diseases like obesity, hypertension, and diabetes. In the last few years, the rise in diabetes cases has coincided with the rapid elevation in obesity rates, resulting in a global health crisis. Major risk factors playing a critical role in the spread of obesity include high-fat food consumption, high-calorie foods, and insufficient physical activity. Diabetes is strongly linked with obesity in terms of metabolic abnormalities and physiological processes, including inflammation. Diabetes type 2 (T2D) is caused primarily by insulin resistance and insufficient insulin release from beta cells of the pancreas. An obese or overweight individual has a strong association with insulin resistance, which in turn leads to the development of T2D. Metabolic stress due to nutrient overload releases different types of inflammatory mediators (such as TNF-α, IL-6, and SFRP4) from adipose tissues in obesity. Secreted frizzled-related protein 4 (SFRP4) is also an inflammatory mediator that impairs insulin secretion. SFRP4 acts as an early biomarker for diabesity expressed with interleukin-1 beta (IL-1β) in the adipose tissues that hinders the exocytosis of insulin-secreting granules from the pancreatic β-cells and is a potential target for preserving β-cell dysfunction and the diabesity treatment. In the current study, plant-based phytocompounds were identified and investigated <em>in silico</em> and <em>in vivo</em> for their ability to suppress the expression of SFRP4. In a diet-induced mouse model, short-listed compounds such as resveratrol and quercetin at higher and lower doses were found effective and significant in reducing the anti-inflammatory mediators and SFRP4 levels. Overall, the current study describes the expression of SFRP4, IL-6, and TNF-α, and its inhibition by various inhibitors. Moreover, the study's findings suggest that resveratrol and quercetin hold promise as potential treatments for diabesity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"761 ","pages":"Article 151748"},"PeriodicalIF":2.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791644","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}
Takamitsu A. Kato , Yoshihiro Fujii , Maeda Junko , Cathy Su , Jeremy S. Haskin , Hirokazu Hirakawa , Akira Fujimori , Paul F. Wilson
{"title":"Cell cycle-dependent radiosensitivity of CHO DNA repair mutants exposed to accelerated charged particles","authors":"Takamitsu A. Kato , Yoshihiro Fujii , Maeda Junko , Cathy Su , Jeremy S. Haskin , Hirokazu Hirakawa , Akira Fujimori , Paul F. Wilson","doi":"10.1016/j.bbrc.2025.151747","DOIUrl":"10.1016/j.bbrc.2025.151747","url":null,"abstract":"<div><div>The two primary DNA double-strand break (DSB) repair pathways, non-homologous end joining (NHEJ) and homologous recombinational repair (HRR), play crucial roles in determining radiosensitivity throughout the cell cycle. Our study investigated mechanisms underlying cell cycle-dependent radiosensitivity following exposure to accelerated charged particles in DSB signaling and repair-deficient CHO mutant cell lines. We confirmed NHEJ-deficient V3 cells exhibit hyper-radiosensitivity across all phases, while HRR-deficient 51D1 cells display increased sensitivity in the typically radioresistant S/G2 phase following X- and gamma-rays. Exposures to accelerated 290 MeV/n C-12 and 500 MeV/n Fe-56 ions induced complex DNA damage that was not fully repaired by either pathway, leading to increased cell killing. HRR-deficient cells exhibited higher relative biological effectiveness (RBE) values for cell killing in G1 and S and levels of chromatid-type chromosomal aberrations were higher in HRR-deficient cells. Additionally, impaired G2-phase checkpoint activation in HRR-deficient cells contributed to mitotic entry with unresolved DNA damage. Our findings suggest that charged particles produce complex lesions that require coordinated repair by both major DSB repair pathways, and disruption of either pathway leads to increased radiosensitivity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"762 ","pages":"Article 151747"},"PeriodicalIF":2.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143791718","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}
Yuling Chen , Ya Xu , Yu Zhang , Danni Yang , Yi Sun
{"title":"Functions of the fusogenic and non-fusogenic activities of Syncytin-1 in human physiological and pathological processes","authors":"Yuling Chen , Ya Xu , Yu Zhang , Danni Yang , Yi Sun","doi":"10.1016/j.bbrc.2025.151746","DOIUrl":"10.1016/j.bbrc.2025.151746","url":null,"abstract":"<div><div>Human endogenous retroviruses (HERVs), which represent the genetic remnants of ancient viral infections, constitute approximately 8 % of the human genome. Among the proteins encoded by these viruses, Syncytin-1, encoded by the <em>env</em> gene of the HERV-W family, functions as a vital fusion protein in placental development, in which it plays a pivotal role in facilitating the fusion of trophoblast cells to form the syncytiotrophoblast that is essential for maintaining the structural integrity and functional viability of the placenta. Recent studies have shown that in addition to its expression in the placenta, Syncytin-1 also plays key roles in a range of different tissues and cell types, influencing biological processes such as cell proliferation, apoptosis, and immune regulation. Abnormal expression of Syncytin-1 has been closely linked to the onset, progression, and metastasis of tumors, potentially promoting tumor invasion via mechanisms involving cell fusion and modulation of the immune microenvironment. Moreover, associations have been established between Syncytin-1 and neurological disorders, including multiple sclerosis and schizophrenia, in which it modulates neuroinflammation. In this review, we systematically examine the molecular structure and functional attributes of Syncytin-1, emphasizing its roles in cell fusion, tumor progression, and immune regulation, and discuss its potential applications as a therapeutic target and diagnostic biomarker.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"761 ","pages":"Article 151746"},"PeriodicalIF":2.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143783462","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":"Exosomal 4EBP1 promotes head and neck cancer progression via regulating mitochondrial fission","authors":"Iyyannar Madhu , Anbarasu Kannan","doi":"10.1016/j.bbrc.2025.151735","DOIUrl":"10.1016/j.bbrc.2025.151735","url":null,"abstract":"<div><div>Head and neck cancer (HNC) is the sixth most common cancer around the globe with raised incidence and mortality. Despite the advancement in diagnostic and therapeutic approaches the burden of HNC has not reduced. Therefore, investigation on key molecular mechanisms that contributes to the progression of HNC is required to identify promising therapeutic targets. Exosomes are nanosized vesicles and recently emerged as a carrier of tumorigenic proteins essential for cancer progression. However, the role of exosomal proteins in HNC progression remains largely unclear. Eukaryotic Initiation Factor 4E-Binding protein 1 (4EBP1) regulates the protein synthesis and plays a crucial role in the progression of different forms of cancer. Our current study revealed that 4EBP1 is carried in human serum exosomes and upregulated in HNC serum exosomes than healthy controls (HC) and we observed that coculturing the 4EBP1 upregulated HNC serum exosomes (HNC Exo) promoted the growth and migration of HEp-2 cells. Further, we examined the underlying mechanism by knockdown of 4EBP1 in HEp-2 cells (4EBP1 KD). Our results showed that knockdown of 4EBP1 have suppressed the migration and progression of cancer cells. Mechanistically, knockdown of 4EBP1 downregulated mitochondrial fission modulators DRP1 and FIS1 and attenuated the migration of HNC cancer cells by suppressing TGFβ and upregulating PTEN. Together our findings suggest that 4EBP1 is upregulated in circulating exosomes and promotes HNC progression via modulating mitochondrial fission and could be a potential therapeutic target for HNC.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"761 ","pages":"Article 151735"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776708","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}