International Journal of Biochemistry & Cell Biology最新文献

{"title":"Critical role of argininosuccinate lyase in TAp73-mediated proliferating tumor cells","authors":"Jie Zhang ,&nbsp;Min Zhao ,&nbsp;Haolan Zhang,&nbsp;Chenjie Ma,&nbsp;Chunyan Ma,&nbsp;Le Li","doi":"10.1016/j.biocel.2025.106803","DOIUrl":"10.1016/j.biocel.2025.106803","url":null,"abstract":"<div><div>The dysregulation of the urea cycle resulting in an excessive buildup of ammonia is identified as a pivotal mechanism driving tumor progression. In particular, argininosuccinate lyase (ASL) is crucial for cancer cell proliferation, cleaves argininosuccinic acid to produce arginine and fumarate in the urea cycle. However, the mechanisms controlling ASL expression in cancer cells remain unclear. Herein, we found that TAp73, a transcription factor within the p53 family, regulates the urea cycle pathway in tumor cells with mutant or null p53. Deletion of TAp73 led to increased accumulation of ammonia and changes in urea cycle metabolites. Subsequent experimentation involving the suppression of TAp73 substantiated its pronounced capability in impeding tumor proliferation and tumorigenicity in both in vitro and in vivo settings. Chromatin immunoprecipitation revealed that TAp73 could bind to specific sequences in the <em>ASL</em> promoter, thus promoting ASL expression, increasing intracellular arginine, and reducing ammonia levels. This investigation undertook a clinical scrutiny of TAp73 expression levels in tumor patients' transcriptomes, revealing an inverse relationship between TAp73 expression and patient survival. These results suggested that TAp73 led to abnormalities in the urea cycle by enhancing ASL expression and will be an important factor in promoting tumor proliferation and a potential target for tumor drugs.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106803"},"PeriodicalIF":3.4,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144095529","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":"Deciphering the molecular heterogeneity of soft tissue sarcoma by integrating multiomics and single cell sequence","authors":"Haixiang Zhang ,&nbsp;Peng Luo ,&nbsp;Hao Jiang ,&nbsp;Aimin Jiang ,&nbsp;Wei Wei ,&nbsp;Chunbiao Wu","doi":"10.1016/j.biocel.2025.106801","DOIUrl":"10.1016/j.biocel.2025.106801","url":null,"abstract":"<div><h3>Background</h3><div>Soft tissue sarcoma is a highly malignant tumor with extensive heterogeneity across multiple omics. However, a comprehensive multi-omics subtyping system has not yet been established.</div></div><div><h3>Methods</h3><div>We integrated sarcoma multi-omics data, including clinical information, transcriptome expression profiles, DNA methylation, and somatic mutations. Using ten advanced clustering algorithms, we identified robust subtypes and validated the reproducibility of our analysis in two independent external datasets. We also identified subtype-specific treatment strategies and analyzed the differences in microenvironments between subtypes using single-cell data.</div></div><div><h3>Results</h3><div>Based on multi-omics subtyping, we identified two novel sarcoma molecular subtypes, named sarcoma multi-omics subtype 1 (SAMS1) and SAMS2. SAMS2 exhibited a poorer prognosis, with significantly activated Myc, glycolysis, and Wnt beta-catenin signaling pathways. SAMS2 was characterized by a lower abundance of immune cell infiltration and anti-tumor immunity deficiency, which owned a lower response rate to immunotherapy but was sensitive to certain targeted drugs, including pazopanib, axitinib, thapsigargin, and elesclomol. MK886 and NU1025 were identified as effective therapeutic targets for the SAMS2. In SAMS2-like tumor epithelial cells, <em>HOXB13</em>/<em>COL16A1</em> and <em>BASP1</em> regulated epithelial-mesenchymal transition. We found that <em>WNT7B</em> was highly expressed in STS and was associated with poor patient prognosis, suggesting its potential as a novel therapeutic target for STS patients.</div></div><div><h3>Conclusion</h3><div>The STS molecular subtyping system based on multi-omics data effectively distinguishes patients with poor prognosis. The subtyping results are robust and reliable, providing new insights for the precise diagnosis and treatment of these patients.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106801"},"PeriodicalIF":3.4,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144089881","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":"Mycobacterium tuberculosis curli pili reduces oxygen consumption rate of THP-1 macrophages during early infection","authors":"Shinese Ashokcoomar ,&nbsp;Tarien J. Naidoo ,&nbsp;Bridgette M. Cumming ,&nbsp;Zainab Baig ,&nbsp;Barry Truebody ,&nbsp;Jared S. Mackenzie ,&nbsp;Adrie J.C. Steyn ,&nbsp;Manormoney Pillay","doi":"10.1016/j.biocel.2025.106802","DOIUrl":"10.1016/j.biocel.2025.106802","url":null,"abstract":"<div><div>The development of improved anti-tuberculosis (TB) strategies to address drug-resistance and ineffectual TB treatment regimens should focus on interrupting the initial host-pathogen interaction. This study aimed to elucidate the effect of surface-located adhesin, <em>Mycobacterium tuberculosis</em> (<em>Mtb</em>) curli pili (MTP), on the bioenergetic and metabolomic profiles of THP-1 macrophages during initial stages of infection. Differentiated THP-1 macrophages were infected with wildtype (WT), ∆<em>mtp</em>, or <em>mtp</em>-complemented strains of <em>Mtb</em>. Bioenergetic profiles and metabolic flux were determined and statistical analysis highlighted differences/similarities amongst the THP-1 macrophage groups. The ∆<em>mtp</em> infected THP-1 macrophages mimicked the higher oxygen consumption rate (OCR) for basal respiration, ATP production, maximal respiration and spare respiratory capacity of the uninfected THP-1 macrophages, relative to the WT and <em>mtp</em>-complement infected THP-1 macrophages. The ∆<em>mtp</em> infected THP-1 macrophages displayed the highest compensatory glycolytic rate. <em>Mtb</em> infection caused the redirection of carbon from the tricarboxylic acid cycle to glycolysis, in addition to an increased flux through the pentose phosphate pathway. However, in the ∆<em>mtp</em> infected THP-1 macrophages, the total metabolite abundance was lower, similar to the uninfected THP-1 macrophages. Data indicates that the absence of MTP facilitates prompt clearance of the intracellular pathogen before it establishes a successful infection. This implies that the presence of MTP facilitates the survival of the pathogen during the early stages until infection is established. These findings support the growing evidence that the MTP adhesin is an important virulence factor and interruption of the interaction between pathogen and host, will facilitate swift clearance of the infection by the host.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106802"},"PeriodicalIF":3.4,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144070670","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":"Silencing HMGB1 secretion inhibited EV71-induced blood-brain barrier dysfunction and neural inflammation by depressing astrocyte activation via sHh signal blockage","authors":"Yufeng Zhang ,&nbsp;Yanfang Liu ,&nbsp;Han Wan ,&nbsp;Huiling Deng ,&nbsp;Pengfei Xu ,&nbsp;Lu Cao ,&nbsp;Xiru Yang ,&nbsp;Hui Li","doi":"10.1016/j.biocel.2025.106797","DOIUrl":"10.1016/j.biocel.2025.106797","url":null,"abstract":"<div><div>It is unclear whether high mobility group protein B1 (HMGB1) is associated with the malignant characterization of hand, foot, and mouth disease (HFMD), and whether it plays a key regulatory role in the process of enterovirus 71 (EV71)-induced brain damage. Firstly, we analyzed the correlation between clinical information and HMGB1 concentrations in patients with mild and severe HFMD. Immunofluorescence was used to determine the expression level of HMGB1 in astrocytes. The levels of cellular inflammatory factors (IL-1β, IL-4, IL-6, TNF-α and TGF-β1), chemokines (CCL2, CXCL10 and CXCL12) and adhesion factors (integrin β, P-gp, VCAM-1 and ICAM-1) were detected by ELISA kits. Western blot was used to measure the levels of blood-brain barrier (BBB) stability related factors (retinoic acid (RA), ANG1, ApoE and IGF-1) in astrocytes and BBB structure related proteins (occluding, claudin, PTCH-1 and ZO-1) in endothelial cells. Clinical studies found that the expression of HMGB1 was closely related to the HFMD severity. Knockdown of HMGB1 alleviated EV71-induced neuron damage and inhibited cellular inflammation and apoptosis. Importantly, silencing HMGB1 depressed excessive proliferation and the inflammation response of astrocytes caused by EV71 infection. Furthermore, knockdown of HMGB1 enhanced BBB stability by improving astrocyte adhesion and endothelial tight junctions. Mechanistically, HMGB1 regulated the stability of BBB by regulating sHh signaling and secretion in astrocytes. In conclusion, the level of HMGB1 is closely related to the clinical symptoms of patients with HFMD, and inhibiting the expression of HMGB1 promotes BBB stability by promoting sHh signaling in astrocytes.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106797"},"PeriodicalIF":3.4,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144046249","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":"Restoration of A2M reduces drug resistance and malignancy in paclitaxel-resistant lung cancer cells","authors":"Xiaona Fan ,&nbsp;Hongsheng Xue ,&nbsp;Ziwei Liu ,&nbsp;Ying Zhou ,&nbsp;Xuying Huang ,&nbsp;Xiaomei Dong ,&nbsp;Qianqian Sun ,&nbsp;Jiannan Yao ,&nbsp;Jian Liu","doi":"10.1016/j.biocel.2025.106789","DOIUrl":"10.1016/j.biocel.2025.106789","url":null,"abstract":"<div><div>The development of acquired paclitaxel resistance poses a significant challenge in managing lung cancer clinically. Understanding the mechanism and developing effective strategies to counter paclitaxel resistance are highly desired. To explore the potential mechanisms of acquired paclitaxel resistance, we established a series of lung cancer cell lines exhibiting different levels of resistance to paclitaxel. Transcriptomic RNA-sequencing revealed a progressive decrease in alpha-2-macroglobulin (A2M) levels as paclitaxel resistance advanced in NCI-H446 cells. This was accompanied by the upregulation of known paclitaxel resistance inducers ABCB1, TMEM243, and ID1. A2M loss was further validated in paclitaxel-resistant A549 and HCC827 lung cancer cells. TCGA and CPTAC analyses demonstrated that A2M is downregulated in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), inversely correlating with tumor progression. Restoring A2M expression inhibited proliferation and invasion in paclitaxel-resistant lung cancer cells, suggesting its tumor-suppressing role in lung cancer. Notably, restoring A2M re-suppressed the expression of the paclitaxel resistance mediators (ABCB1, TMEM243 and ID1) in the drug-resistant cells, and re-sensitized them to paclitaxel. In summary, our data indicate that A2M is progressively lost during the development of paclitaxel resistance in lung cancer, and restoring A2M may help overcome this resistance. Thus, A2M deficiency may serve as both a predictor and a therapeutic target for paclitaxel resistance in lung cancer.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106789"},"PeriodicalIF":3.4,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143929467","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":"Single-cell transcriptomics and metabolomics reveal the potential role of ASRGL1 in metabolic reprogramming and invasion of nasopharyngeal carcinoma cells","authors":"YingYing Pei ,&nbsp;Chunlin Li ,&nbsp;Bin Zhang ,&nbsp;Qi Zheng ,&nbsp;Shengnan Chen ,&nbsp;Ji Li","doi":"10.1016/j.biocel.2025.106788","DOIUrl":"10.1016/j.biocel.2025.106788","url":null,"abstract":"<div><div>Nasopharyngeal carcinoma (NPC) is an aggressive and highly metastatic malignancy, presenting significant challenges for early diagnosis and treatment. Asparaginase-like protein 1 (ASRGL1) is an important enzyme involved in amino acid metabolism, and previous studies have linked it to the progression of various tumors. However, the specific role of ASRGL1 in NPC remains unclear. This study analyzed multiple publicly available datasets related to NPC. We conducted single-cell RNA sequencing (scRNA-seq) analysis on the GSE150430 dataset to identify different cell subpopulations and examine ASRGL1 expression and its functional implications. The expression of ASRGL1 and its correlation with EMT were validated using transcriptomic data. The expression of ASRGL1 in C666–1 cells was interfered with by siRNA, cell proliferation and invasion were detected by CCK8, EdU, plate cloning, Transwell and scratch method, and EMT was evaluated by detecting the expression of E-cadherin and N-cadherin. Amino acid metabolomics and GC-MS headspace metabolomics were used to analyze the effects of ASRGL1 knockdown on the metabolic pattern of NPC cells. This study found that ASRGL1 was mainly expressed in fibroblasts, epithelial cells and myeloid cells in nasopharyngeal carcinoma (NPC). The ASRGL1-cell gene was significantly enriched in the epithelial-mesenchymal transition pathway. Knocking down ASRGL1 can further inhibit the proliferation, invasion and EMT of C666–1 cells. At the same time, the utilization of various amino acids was significantly reduced, and further GC-MS metabolomics analysis showed that the cell metabolism was unbalanced. This study elucidates the expression characteristics and potential functional roles of asparaginase-like protein 1 (ASRGL1) in nasopharyngeal carcinoma (NPC), providing new insights into its potential as a diagnostic marker and therapeutic target.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106788"},"PeriodicalIF":3.4,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143922373","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":"Acalabrutinib alleviates metabolic dysfunction–associated steatotic liver disease by regulating bile acid metabolism","authors":"Yanbo Wang,&nbsp;Shiwei Chen,&nbsp;Bingjue Ye,&nbsp;Zhenggang Yang,&nbsp;Yanning Liu,&nbsp;Guohua Lou,&nbsp;Cheng Zhou,&nbsp;Min Zheng","doi":"10.1016/j.biocel.2025.106786","DOIUrl":"10.1016/j.biocel.2025.106786","url":null,"abstract":"<div><div>Metabolic dysfunction–associated steatotic liver disease (MASLD) is a global epidemic of chronic liver disease currently lacking effective treatment. Evaluating the therapeutic effects of existing drugs on MASLD is a time and cost-effective strategy. Bruton's tyrosine kinase (BTK) is an inflammatory signaling molecule playing an important role in the progression of MASLD. Aclabrutinib, a BTK inhibitor approved for treating mantle-cell lymphoma and chronic lymphocytic leukemia, has not been investigated for its potential to treat MASLD. This study examined the therapeutic effects and mechanisms of aclabrutinib on MASLD using a high-fat diet-induced mouse model. Results demonstrated significant alleviation of pathological parameters associated with MASLD upon administration of aclabrutinib. TSE PhenoMaster results revealed that aclabrutinib increased energy expenditure in mice. Furthermore, aclabrutinib upregulated the expression of genes associated with thermogenesis and lipolysis in adipose tissues. Additionally, it inhibited the transcription of genes related to lipid absorption in the small intestine and liver, while increasing the expression of hormone-sensitive lipase, hepatic nuclear factor 4 alpha and fibroblast growth factor 21 in the liver. Further analysis indicated that aclabrutinib promoted the alternative pathway of bile acid synthesis while restoring gut microbiota homeostasis. The altered bile acid profiles upregulated G protein-coupled bile acid receptor 1 expression in adipose tissues as well as vitamin D receptor expression in liver and small intestine. Our findings suggest that by regulating bile acid metabolism and gut microbiota, aclabrutinib may promote thermogenesis and lipolysis, thereby alleviating MASLD. This study provides novel insights into clinical applications targeting BTK for treating MASLD.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106786"},"PeriodicalIF":3.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947136","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":"Morin inhibits the progression of 5-fluorouracil–resistant colorectal cancer by suppressing autophagy","authors":"Rui Li ,&nbsp;Fengxia Wang ,&nbsp;Lu Huang ,&nbsp;Lvheng Zhao ,&nbsp;Ting Qin ,&nbsp;Shan Liu ,&nbsp;Kunyao Xu ,&nbsp;Bi Wang ,&nbsp;Ling Li ,&nbsp;Sha He","doi":"10.1016/j.biocel.2025.106783","DOIUrl":"10.1016/j.biocel.2025.106783","url":null,"abstract":"<div><h3>Background</h3><div>Resistance to 5-fluorouracil (5-FU) poses a significant challenge in colorectal cancer (CRC) treatment. Morin is a flavonoid with anti-tumor properties. However, its role in overcoming acquired 5-FU resistance in CRC remains unclear.</div></div><div><h3>Methods</h3><div>5-FU-resistant CRC (5-FU/CRC) cell lines (HT29/5-FU and HCT116/5-FU) were established using the IC50 concentration increment method. After treatment with Morin and autophagy inhibitors (3-MA) or agonists (RAPA), cell viability, apoptosis, colony formation, migration, invasion, and autophagy were evaluated. <em>In vivo</em>, xenograft models of 5-FU/CRC assessed Morin's therapeutic effects.</div></div><div><h3>Results</h3><div>5-FU/CRC cells were successfully constructed. Morin inhibited the viability, migration, and invasion of 5-FU/CRC cells and promoted apoptosis. Morin also inhibited autophagy in 5-FU/CRC cells. Besides, autophagy activated by RAPA could eliminate the effect of Morin on 5-FU/CRC cells, while 3-MA enhanced the effects of Morin. In nude mouse models, Morin inhibited the growth and improved the pathological structure of 5-FU/CRC xenografts by inhibiting autophagy.</div></div><div><h3>Conclusion</h3><div>Morin suppresses the progression of 5-FU/CRC by inhibiting autophagy, suggesting its potential as a therapeutic agent to combat 5-FU resistance.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106783"},"PeriodicalIF":3.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143940976","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":"Inhibition of M2 macrophage-mediated mesenchymal stem cell migration: Boldine attenuates elbow heterotopic ossification","authors":"Fengteng Shen ,&nbsp;Yansong Chen ,&nbsp;Zhikun Xu ,&nbsp;Wei Wang ,&nbsp;Guofang Chen ,&nbsp;Fusheng Ye","doi":"10.1016/j.biocel.2025.106787","DOIUrl":"10.1016/j.biocel.2025.106787","url":null,"abstract":"<div><h3>Background</h3><div>Heterotopic ossification (HO) is characterized by abnormal bone formation in soft tissues, often following trauma or surgery. Transforming growth factor-beta (TGF-β) signaling and M2 macrophage polarization play critical roles in the recruitment and differentiation of mesenchymal stromal/progenitor cells (MSPCs), promoting HO.</div></div><div><h3>Methods</h3><div>An elbow joint trauma-induced HO mouse model was established, where model mice were treated with dichloromethylene-bisphosphonate (Cl2MBP) liposomes or PBS liposomes to deplete macrophages. In addition, boldine was administered to evaluate its therapeutic effect on HO formation. Bone marrow mesenchymal stem cells (BMSCs) were also extracted for <em>in vitro</em> experiments. Quantitative real-time PCR (qRT-PCR) and Western blot were conducted to assess gene and protein expression. <em>In vivo</em> methods included Micro-Computed Tomography (Micro-CT) to assess bone formation, histological staining to evaluate tissue changes, immunohistochemistry (IHC) and immunofluorescence to analyze macrophage, CD73⁺ and CD105⁺ cells infiltration. <em>In vitro</em>, BMSCs were identified by flow cytometry and treated with interleukin-10 (IL-10) and/or boldine, and assays such as cell viability (Cell Counting Kit 8 (CCK8)), migration (Transwell), immunofluorescence, ALP staining, and Alizarin Red S staining, were conducted to assess osteogenic differentiation.</div></div><div><h3>Results</h3><div>Boldine treatment significantly reduced HO formation, decreased collagen deposition, and inhibited M2 macrophage infiltration (<em>P</em> &lt; 0.05). <em>In vitro</em>, boldine reduced IL-10-induced cell activity, migration, and osteogenic differentiation of BMSCs and inhibited TGF-β and pSmad2/3/Smad2/3 protein (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Boldine attenuates HO by inhibiting M2 macrophage-mediated MSPC migration and might involve the TGF-β signaling, suggesting its potential as a therapeutic approach for managing HO.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"185 ","pages":"Article 106787"},"PeriodicalIF":3.4,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886988","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":"Association of long non-coding RNA in lipid metabolism: Implications in leukemia","authors":"Anjani Alluri ,&nbsp;Pallavi Saxena ,&nbsp;Amit Mishra ,&nbsp;Ravi Kumar Gutti","doi":"10.1016/j.biocel.2025.106785","DOIUrl":"10.1016/j.biocel.2025.106785","url":null,"abstract":"<div><div>Cancer has high mortality rate and occupies second position among major diseases. Despite extensive research and therapies, in every nook and corner of the world, death rate is increasing exponentially. Hallmarks of cancer are benchmarks of cancer cells describing the fundamental principle and capabilities of the cells transforming from normal to malignant tumour. One of the major ones among them is the deregulation of cellular metabolism or metabolic reprogramming, involving alterations in glucose and lipid metabolism. Progressive research in this area has visualized the vital role of lncRNAs in lipid metabolism with respect to AML. lncRNAs involve in various cellular processes and also contribute for significant functions of the cell like chromatin remodelling, transcriptional activation and repression, gene regulation, immune response, cell differentiation, and cell cycle regulation, in addition to oncogenic processes such as proliferation, angiogenesis, migration, and apoptosis. Structural similarities are observed among mRNAs and lncRNAs in terms of poly A-tail and 5^’ cap however protein-coding regions are lacking. A large body of evidence has shown that lncRNAs directly or indirectly mediate lipid metabolism by activating downstream genes. Considering their potential involvement in leukemia, these lncRNAs can be explored and considered as biomarkers for therapeutics, prognosis, and diagnosis. The present review is planned to summarize the functional classification of lncRNAs, the role of lipid metabolism in cancer, different lncRNAs involved in leukemia, and different cancer types related to lipid metabolism.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"184 ","pages":"Article 106785"},"PeriodicalIF":3.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848436","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}