Iranian Journal of Biotechnology最新文献

{"title":"MiRNA-Based Exosome-Targeted Multi-Target, A Multi-Pathway Intervention for Personalized Lung Cancer Therapy: Prognostic Prediction and Survival Risk Assessment.","authors":"Jiefeng Liu, Yukai Tang, Xueying Liu, Yujing Gong, Ziqi Sun, Yao Yin, Yiping Liu","doi":"10.30498/ijb.2025.516588.4112","DOIUrl":"10.30498/ijb.2025.516588.4112","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer remains one of the most prevalent and lethal cancers globally, often diagnosed at advanced stages, which impedes effective treatment. Recent advancements have highlighted exosomes as valuable biomarkers for early detection, prognosis, and therapeutic interventions in lung cancer. Exosomes, which carry molecular information from tumor cells, reflect tumor development and metastasis, offering potential for precision medicine.</p><p><strong>Objective: </strong>This study aimed to develop a prognostic prediction model for lung cancer therapy based on miRNA profiling in exosomes. By performing bioinformatics analyses, we identified miRNAs and target genes associated with lung cancer treatment and their potential relationship with patient survival outcomes.</p><p><strong>Materials and methods: </strong>Using the GSE207715 dataset, we applied machine learning models and a Transformer-based deep learning approach to predict nivolumab treatment efficacy in lung cancer patients. Additionally, miRNA-target gene interactions were predicted via miRNA databases, followed by Gene Ontology and KEGG pathway enrichment analyses. A Cox proportional hazards regression model was used to assess the relationship between miRNA expression and patient survival.</p><p><strong>Results: </strong>Significant differences were observed in the miRNA profiles of exosomes from patients with different nivolumab treatment outcomes, though the differences were relatively small. Machine learning models achieved prediction accuracies ranging from 0.6731 to 0.6923, while the deep learning model outperformed these methods with an accuracy of 0.9412. The hsa-let-7c miRNA showed statistical significance in multivariate survival risk analysis (p = 0.0152).</p><p><strong>Conclusion: </strong>This study demonstrates the potential of miRNA profiling in exosomes for predicting treatment efficacy and survival in lung cancer patients. The deep learning model's ability to capture subtle miRNA expression differences provides a robust platform for personalized treatment strategies in non-small cell lung cancer.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4112"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the Safety of A Novel Anti-HER2 Immunotoxin Containing Modified Fragment of <i>Pseudomonas</i> Exotoxin in BALB/C Mice.","authors":"Fatemeh Saadatkhah, Valiollah Hajhashemi, Azar Naimi, Vajihe Akbari, Melika Kolahdoozan","doi":"10.30498/ijb.2025.481960.4000","DOIUrl":"10.30498/ijb.2025.481960.4000","url":null,"abstract":"<p><strong>Background: </strong>Human epidermal growth factor-2 (HER-2) receptors are overexpressed in some malignancies like breast cancer. Previously, we constructed a novel anti-HER immunotoxin, scFv-PE35KDEL, containing modified fragments of <i>Pseudomonas</i> exotoxin, which showed remarkable <i>in vitro</i> cytotoxicity against breast cancer cells. <i>In vivo</i> safety evaluation is essential for evaluating toxicity to perform <i>in vivo</i> efficacy studies. This study aimed to evaluate the acute toxicity of scFv-PE35KDEL in BALB/c mice.</p><p><strong>Objectives: </strong>The objective of this research was to express and purify the recombinant scFv-PE35KDEL protein and remove its endotoxin content, as well as to evaluate its toxicity profile by determining the LD₅₀ and monitoring body weight changes in BALB/c mice following injection.</p><p><strong>Materials and methods: </strong>After expression and purification of scFv-PE35KDEL, BALB/c mice were intraperitoneally administered single doses of 250, 500, 1000, and 2000 µg.kg^-1 of immunotoxin. Mice's weight, body temperature, and acute toxicity symptoms were evaluated every odd day for two weeks. Histopathological evaluation of the kidney, liver and lungs was performed.</p><p><strong>Results: </strong>All mice died after a single dose of 2000 µg.kg^-1 of immunotoxin, but after exposure to 1000 µg.mg^-1, all mice survived for 15 days. There was no significant difference in the body temperature between the groups (<i>p</i> > 0.05). There was a considerable weight loss at 500 and 1000 µg.kg^-1 doses until three days (<i>p</i> < 0.05) which recovered gradually. Diarrhea and loss of muscular tonicity were among the common adverse effects, which were worsened by increasing the dose to 1000 µg.mg^-1. Based on histopathological analysis, no specific toxicity was observed in the liver and kidney tissues at doses up to 1000 µg.kg^-1.</p><p><strong>Conclusion: </strong>These findings revealed that the LD50 of scFv-PE35KDEL is in the range of 1000-2000 µg.mg^-1 and it seems to be a safe and non-toxic agent, and could be a promising candidate for anti-HER2 cancer therapy. However, further <i>in vivo</i> evaluations are required.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4000"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374125/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the Effect of Environmental Factors on Production of Microalgae <i>Nannochloropsis Oculata</i> in A Vertical Photo Bioreactor.","authors":"Mohammad Hossein Afsharbakhsh, Ahmad Mohammadi, Hamid Mashhadi, Fahimeh Mahmoudnia","doi":"10.30498/ijb.2025.479547.3995","DOIUrl":"10.30498/ijb.2025.479547.3995","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Microalgae like &lt;i&gt;Nannochloropsis oculata&lt;/i&gt; are gaining interest in biotech for sustainable biofuels and nutrition due to their lipid and protein production. This study explores how factors like light, temperature, pH, and nutrients affect &lt;i&gt;N. oculata&lt;/i&gt;'s growth and productivity to enhance bioprocesses.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;The goal was to refine these environmental conditions to enhance the biotechnological applications of &lt;i&gt;N. oculata&lt;/i&gt; , fostering innovative solutions in sustainable energy and nutrition.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Materials and method: &lt;/strong&gt;This study examined how culture medium, temperature, pH, and light affect biomass, chlorophyll, carotenoids, and lipid content of &lt;i&gt;Nannochloropsis oculata&lt;/i&gt; in a photobioreactor. A light intensity of 5000 Lux was used for 16 hours with three medium: Walne, BBM, and Jourdan. Temperatures of 25 °C and 30 °C, and pH levels of 7-9 and 9-11 were tested. Key outcomes included cell density, growth rate, biomass, and lipid production, analyzed using Design Expert.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The study conducted highlighted notable and significant discrepancies in various parameters, specifically cell density (measured in cells.mL&lt;sup&gt;-1&lt;/sup&gt;), biomass (expressed in g.L&lt;sup&gt;-1&lt;/sup&gt;), and chlorophyll content across the three different culture media: Walne, BBM, and Jordan. These differences were statistically validated at a significance level of 1%, all while maintaining carefully controlled conditions for temperature and pH. Among the three, Walne medium produced the most favorable outcomes for the growth of &lt;i&gt;N. oculata&lt;/i&gt; , particularly when cultured at a pH level of 9 and at a temperature of 25 °C. This medium clearly outperformed the others in terms of biological performance metrics. On the other hand, Jordan medium emerged as the more economically viable option for large-scale cultivation despite the superior biological results associated with Walne. Not only was Jordan medium financially advantageous, but it also demonstrated remarkable lipid production capabilities, with Palmitic acid identified as the predominant fatty acid present in the cultures grown in this medium. Furthermore, the investigation revealed that both temperature and pH have a significant and impactful role in regulating the production of chlorophyll and carotenoids. This finding emphasizes the critical importance of maintaining optimal culture conditions in order to maximize the metabolic production efficiency of microalgae.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;In conclusion, the selection of the appropriate culture medium plays a crucial role in influencing both the growth metrics and biochemical performance of &lt;i&gt;N. oculata&lt;/i&gt;. Specifically, Walne medium attained the highest measures for cell density, biomass accumulation, and chlorophyll production when cultivated under the optimal conditions of pH 9 and 25 °C. Although Walne medium provides superior biological res","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e3995"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biotechnological Insights into LncRNA-STAT3 Interactions: A Novel Diagnostic Biomarker for Myocardial Hypertrophy.","authors":"Guangmei Zou","doi":"10.30498/ijb.2025.515128.4104","DOIUrl":"10.30498/ijb.2025.515128.4104","url":null,"abstract":"<p><strong>Background: </strong>Advances in molecular biology have highlighted the significant role of long non-coding RNAs (lncRNAs) in cardiovascular diseases, including myocardial hypertrophy (MH). This study integrates bioinformatics analysis with molecular validation to investigate the regulatory mechanism of lncRNA ENST00000500113.1 on STAT3 expression, aiming to identify novel biomarkers for MH diagnosis.</p><p><strong>Objectives: </strong>We aimed to explore differential expression patterns of lncRNAs and mRNAs in myocardial hypertrophy using biotechnological approaches and establish their potential as diagnostic and therapeutic targets. The study aims to provide actionable insights that can facilitate the development of biotechnological tools for early diagnosis and intervention in myocardial hypertrophy.</p><p><strong>Materials and methods: </strong>Myocardial tissues from organ donor patients were classified into control and hypertrophy groups. RNA sequencing was performed to identify differentially expressed genes. Advanced bioinformatics techniques were applied for functional enrichment analysis and co-expression network construction. Validation was conducted using qRT-PCR and immunohistochemistry.</p><p><strong>Results: </strong>Bioinformatics analyses revealed that MH-associated mRNAs were enriched in immune system processes and the JAK/STAT signaling pathway. Downregulation of lncRNA ENST00000500113.1 in MH tissues was correlated with upregulated STAT3 expression. Molecular validation confirmed a significant association between ENST00000500113.1 and STAT3, suggesting a regulatory mechanism contributing to MH progression.</p><p><strong>Conclusions: </strong>This study demonstrated the biotechnological potential of integrating bioinformatics and molecular validation to identify lncRNA ENST00000500113.1 as a novel diagnostic biomarker for MH. These findings offer actionable insights into MH pathophysiology and facilitate the development of targeted interventions.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4104"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Significance of <i>E2F8, LIN28b, MACC1</i>, and <i>CCT3</i> Genes in Breast Cancer: Implications for Survival and Therapeutic Stratification.","authors":"Mahdi Alizadeh, Mahdieh Salimi, Zahra Soheila Soheili","doi":"10.30498/ijb.2025.497569.4051","DOIUrl":"10.30498/ijb.2025.497569.4051","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer remains a leading cause of cancer-related mortality among women, highlighting the urgent need for reliable biomarkers that can aid in prognosis and therapeutic stratification.</p><p><strong>Objectives: </strong>This study aimed to evaluate the RNA expression levels of four specific genes-<i>E2F8</i>, <i>LIN28b</i>, <i>MACC1</i>, and <i>CCT3</i>-in breast cancer tumors compared to adjacent normal tissues, and to assess their prognostic significance in relation to clinical parameters and recurrence-free survival.</p><p><strong>Materials and methods: </strong>The RNA expression levels of <i>E2F8</i>, <i>LIN28b</i>, <i>MACC1</i>, and <i>CCT3</i> were examined using SYBR Green real-time PCR. Gene expression data were correlated with clinical parameters, including disease stage, lymph node involvement, and triple-negative status. Survival analysis was conducted to evaluate the prognostic significance of these genes concerning recurrence within five years post-diagnosis, with median expression cutoffs established for each gene and the overall median for the panel. Kaplan-Meier survival analysis was employed to assess the relationship between gene expression and recurrence-free survival, calculating hazard ratios (HR) for each gene and the combined panel. Additionally, the Reactome database was analyzed to identify biological pathways associated with these genes.</p><p><strong>Results: </strong>All four genes demonstrated significantly higher expression levels in breast cancer samples, correlating with advanced disease stages, lymph node involvement, and triple-negative breast cancer status. <i>E2F8</i> expression was notably associated with estrogen receptor (ER) and progesterone receptor (PR) positivity, while <i>MACC1</i> expression correlated with ER negativity. Survival analysis revealed that 6 out of 40 patients expired within five years. Kaplan-Meier analysis indicated that higher expression levels of <i>E2F8</i> (HR 14.80, p=0.0015), <i>LIN28b</i> (HR 9.259, p=0.0071), <i>MACC1</i> (HR 12.49, p=0.0027), and <i>CCT3</i> (HR 7.315, p=0.0158) were significantly associated with reduced recurrence-free survival. The hazard ratio for the combined gene panel was 15.367 (p<0.0001). Reactome analysis revealed that these genes are involved in critical biological pathways, including actin folding by CCT TriC and TP53 regulation of G1 cell cycle arrest.</p><p><strong>Conclusions: </strong>Our findings suggest that this four-gene panel holds significant promise as a robust prognostic tool for breast cancer survival. This research paves the way for further investigations into targeted therapies and personalized medicine approaches in the management of breast cancer.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4051"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Validation of Genes Involved in Energy Metabolism in Polycystic Ovary Syndrome.","authors":"Jinglei Zhang, Huiying Jie, Qingyun Mai, Lin Chen, Canquan Zhou","doi":"10.30498/ijb.2025.514574.4102","DOIUrl":"10.30498/ijb.2025.514574.4102","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysregulation plays a critical role in polycystic ovary syndrome (PCOS), yet the involvement of energy metabolism-related genes (ERGs) remains incompletely understood. This study employs integrative bioinformatics and experimental validation to identify key ERGs as potential biomarkers and therapeutic targets in PCOS.</p><p><strong>Objectives: </strong>This study aimed to screen and validate ERGs associated with PCOS by integrating gene expression datasets (GSE34526 and GSE193123) and to explore their molecular mechanisms and therapeutic implications.</p><p><strong>Materials and methods: </strong>Differentially expressed genes (DEGs) were identified from two GEO datasets and intersected with ERGs from the Reactome database. Functional enrichment, subcellular localization, transcriptional and post-transcriptional regulatory networks, and drug prediction analyses were performed. Clinical validation of candidate biomarkers was conducted using RT-qPCR on granulosa cells from PCOS patients and controls.</p><p><strong>Results: </strong>A total of 159 common DEGs were identified, including three key biomarkers: CD44 (upregulated), HS2ST1, and GPC4 (downregulated). CD44 was localized primarily to the plasma membrane, while HS2ST1 and GPC4 were localized to the Golgi apparatus and nucleus/plasma membrane, respectively. Regulatory network analyses revealed multiple transcription factors, kinases, and miRNAs associated with these biomarkers. Drug prediction identified bisphenol A as a compound linked to all three genes. RT-qPCR confirmed significant upregulation of CD44 in clinical PCOS samples (P<0.05).</p><p><strong>Conclusion: </strong>This study identifies and validates three ERG-associated biomarkers with potential diagnostic and therapeutic utility in PCOS. The integration of bioinformatics and clinical validation underscores the translational relevance of these findings for advancing biotechnological applications in PCOS management.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4102"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eicosapentaenoic Acid Modulates TGF-β1/Smad3/ILK Pathway to Attenuate Renal Fibrosis: A Biotechnological Approach.","authors":"Zhiqiang Wei, Hao Ding, Haitao Li, Di Yin, Juan Cao","doi":"10.30498/ijb.2025.513787.4098","DOIUrl":"10.30498/ijb.2025.513787.4098","url":null,"abstract":"<p><strong>Background: </strong>Renal fibrosis is a key pathological process in chronic kidney disease (CKD), characterized by excessive extracellular matrix (ECM) deposition and epithelial-mesenchymal transition (EMT). Current treatment strategies have limited efficacy, necessitating the exploration of novel therapeutic agents. Eicosapentaenoic acid (EPA), a bioactive marine-derived omega-3 polyunsaturated fatty acid, has shown promise in modulating fibrosis-related signaling pathways.</p><p><strong>Objectives: </strong>This study investigated the potential of EPA in mitigating renal fibrosis through the regulation of the transforming growth factor-β1 (TGF-β1)/Smad3/ILK pathway and its effects on ECM remodeling and EMT suppression in human kidney epithelial cells.</p><p><strong>Materials and methods: </strong>Human Kidney-2 (HK-2) cells were subjected to albumin-induced EMT and treated with EPA, either alone or in combination with the β-catenin inhibitor LF3. The expression levels of key EMT markers (E-cadherin, N-cadherin, vimentin), ECM regulators (MMPs and TIMPs), and fibrosis-related signaling molecules (TGF-β1, Smad3, ILK) were assessed using immunofluorescence, ELISA, RT-qPCR, and Western blot analysis.</p><p><strong>Results: </strong>EPA treatment significantly inhibited EMT by downregulating α-SMA, N-cadherin, vimentin, and active β-catenin while restoring E-cadherin expression (p < 0.05). ECM remodeling was evident through increased MMP-1, MMP-3, and MMP-9 expression and decreased TIMP-1 and TIMP-2 levels. Furthermore, EPA reduced TGF-β1, ILK, and phosphorylated Smad3 protein levels, an effect enhanced by LF3 co-treatment.</p><p><strong>Conclusion: </strong>EPA shows preliminary potential as an antifibrotic agent in vitro by targeting the TGF-β1/Smad3/ILK pathway to regulate ECM remodeling and EMT suppression in renal fibrosis. This study provides insights into the EPA's application in medical biotechnology, particularly for CKD management.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4098"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SP1-Induced LncRNA ZFAS1 Contributes to Cell Proliferation and Migration in Gastric Cancer through AKT/mTOR Signaling.","authors":"Ying Li, Yu Wang, Jun Gao, Weiran Xu, Yingkai Wang, Fan Zhang","doi":"10.30498/ijb.2025.504573.4071","DOIUrl":"10.30498/ijb.2025.504573.4071","url":null,"abstract":"<p><strong>Background: </strong></p><p><strong>Objectives: </strong>This study aimed to investigate the role of lncRNA ZFAS1 in gastric cancer progression, focusing on its regulation by SP1 and its impact on the AKT/mTOR signaling pathway. By exploring ZFAS1's effects on cell proliferation, migration, and apoptosis, we sought to uncover its molecular mechanisms and potential as a therapeutic target.</p><p><strong>Materials and methods: </strong>We evaluated ZFAS1 expression in gastric cancer cells (SGC7901) by RT-qPCR and compared it with GES-1 cells. The LnCAR database provided insight into ZFAS1 levels in STAD compared to normal tissue. To knockdown ZFAS1 in SGC7901 cells, we transfected the cells with si-ZFAS1 #1-3 (small interfering RNAs targeting ZFAS1), and si-ZFAS1-2 was found to have the highest knockdown efficiency. Then, the effect of ZFAS1 knockdown on cell invasion, migration and proliferation was evaluated using transwell invasion, wound healing assays, CCK8 and flow cytometry. In addition, ZFAS1 promoter regions were examined using the JASPAR database and subsequent ChIP assays to understand SP1 transcription factor binding. The effect of ZFAS1 on the AKT/mTOR pathway was clarified using Western blotting.</p><p><strong>Results: </strong>SGC7901 cells were shown to have increased ZFAS1 expression, which was linked to a poor prognosis for gastric cancer. Knockdown of ZFAS1 in SGC7901 cells inhibited cell invasion, migration and proliferation and induced apoptosis. In addition, SP1 was found to upregulate ZFAS1 transcription by binding to its promoter region. ZFAS1 knockdown resulted in a significant reduction of AKT/mTOR pathway components, including p-AKT, AKT, p-mTOR, and mTOR. When the AKT activator SC79 was introduced, the repressive effects of ZFAS1 knockdown on cell invasion, migration, proliferation, and AKT/mTOR signaling were partially reversed.</p><p><strong>Conclusions: </strong>Our results highlight the pivotal role of ZFAS1 in gastric cancer cell malignancy, which inhibits the activation of the AKT/mTOR pathway. The regulatory involvement of SP1 in ZFAS1 transcription provides a novel understanding of the molecular mechanisms driving cancer progression and offers potential therapeutic avenues by suggesting that further research could focus on developing targeted therapies that modulate ZFAS1 expression or activity, which may lead to more effective treatment options for gastric cancer patients in the future.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4071"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biotechnological Elucidation of Xinyin Tablet's Mechanism: SIRT1 Activation Attenuates Cardiac Fibrosis Via Suppressing Endothelial-to-Mesenchymal Transition.","authors":"Qiao Li, Taochun Ye, Qingmin Chu, Xin Shang, Min Liu","doi":"10.30498/ijb.2025.510746.4086","DOIUrl":"10.30498/ijb.2025.510746.4086","url":null,"abstract":"<p><strong>Background: </strong>Xinyin tablet (XYT), a traditional Chinese medicine consisting of <i>Ginseng</i>, <i>Ophiopogon</i>, <i>Astragalus</i>, <i>Ilex pubescens</i>, <i>Motherwort</i>, and other medicines, is clinically used to manage chronic heart failure (HF), yet its molecular mechanisms remain underexplored.</p><p><strong>Objectives: </strong>This study integrates biotechnological approaches to investigate how XYT mitigates cardiac fibrosis by targeting the SIRT1-mediated TGF-β/Smad signaling pathway.</p><p><strong>Materials and methods: </strong>Transverse aortic constriction (TAC)-induced HF mice and TGF-β1-stimulated myocardial microvascular endothelial cells (MMECs) were employed. Echocardiography, histopathology, and molecular assays (qRT-PCR, Western blotting, siRNA transfection) were utilized to assess cardiac function, fibrosis, and signaling pathways.</p><p><strong>Results: </strong>XYT treatment significantly improved cardiac function (↑LVEF, LVFS; ↓LVIDs, LVIDd) and reduced collagen I/III deposition in TAC mice. Mechanistically, XYT upregulated SIRT1 expression while suppressing EndMT markers (↓α-SMA, ↑VE-cadherin) and TGF-β/Smad signaling (↓TGF-βR1, p-Smad2/3). Crucially, SIRT1 knockdown in MMECs abolished XYT's inhibitory effects on EndMT and TGF-β/Smad activation, confirming SIRT1's pivotal role.</p><p><strong>Conclusions: </strong>These findings highlight XYT's biotechnological relevance by linking SIRT1 activation to EndMT inhibition, offering a novel therapeutic strategy for cardiac fibrosis. This study underscores the potential of integrating traditional medicine with molecular biotechnology to develop targeted therapies for cardiovascular diseases.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 2","pages":"e4086"},"PeriodicalIF":1.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144954395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Validation of the Mechanism of Action of TYROBP Related to Blood-Brain Barrier Function in Intracerebral Hemorrhage by Bioinformatics Analysis.","authors":"Chengyuan Ji, Dejing Cheng, Siyuan Yang, Zhong Wang","doi":"10.30498/ijb.2025.487125.4019","DOIUrl":"10.30498/ijb.2025.487125.4019","url":null,"abstract":"<p><strong>Background: </strong>Intracerebral hemorrhage (ICH) is an extremely common acute vascular disease in the elderly population with a high potential for disability and death.</p><p><strong>Objective: </strong>To analyze TYROBP related to blood-brain barrier (BBB) function in ICH through online databases, and to explore their mechanisms of action.</p><p><strong>Materials and methods: </strong>The GSE24265 dataset was chosen for GEO2R analysis, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses. It was discovered that TYROBP was related to the \"maintenance of permeability of BBB\". Subsequently, ICH rat models were constructed, and TYROBP expression in ICH was verified. Lentivirus vectors with abnormally expressed TYROBP were constructed and intervened in ICH rats. The cognitive and learning abilities of rats were tested by the Morris water maze test, and the pathological damage, inflammatory reactions, and oxidative stress responses of brain tissue were detected. Finally, the BBB and microglial pyroptosis in rats were evaluated.</p><p><strong>Results: </strong>Analysis of the GSE24265 dataset showed upregulation of TYROBP, which was also elevated in ICH rats. After enhancing TYROBP expression, the learning and cognitive abilities of ICH rats were further deteriorated, the pathological damage of brain tissues was aggravated, and the BBB leakage and microglial pyroptosis were intensified; silencing TYROBP expression led to completely reversed pathological processes.</p><p><strong>Conclusions: </strong>TYROBP promotes the pathological progression of ICH by increasing the BBB permeability and facilitating microglial pyroptosis.</p>","PeriodicalId":14492,"journal":{"name":"Iranian Journal of Biotechnology","volume":"23 1","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12128946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}