Journal of Biochemical and Molecular Toxicology最新文献

{"title":"Evaluation of Anti-Inflammatory and Antioxidant Effects of Ferulic Acid and Quinic Acid on Acetic Acid-Induced Ulcerative Colitis in Rats","authors":"Mahsa Ekhtiar,&nbsp;Maryam Ghasemi-Dehnoo,&nbsp;Fatemeh Azadegan-Dehkordi,&nbsp;Nader Bagheri","doi":"10.1002/jbt.70169","DOIUrl":"https://doi.org/10.1002/jbt.70169","url":null,"abstract":"<div>\u0000 \u0000 <p>Ulcerative colitis is a chronic inflammatory disease characterized by oxidative stress and the production of pro-inflammatory cytokines. Ferulic acid and quinic acid, two phenolic compounds, are thought to have potent antioxidant and anti-inflammatory properties. This study aimed to investigate the anti-inflammatory and antioxidant effects of ferulic acid and quinic acid in rats with acetic acid (AA)-induced ulcerative colitis. To this end, 64 Wistar rats were randomly divided into eight groups, each consisting of eight rats. AA was administered intrarectally to induce ulcerative colitis. Ferulic acid (20, 40, and 60 mg/kg), quinic acid (10, 30, 60, and 100 mg/kg), and dexamethasone (2 mg/kg) were received daily for five consecutive days. Then, the macroscopic and histopathological changes in the colon tissue were examined. Finally, the tissue levels of heme oxygenase 1 (HO1), nuclear factor erythroid 2-related factor 2 (NRF2), and NAD(P)H quinone dehydrogenase 1 (NQO1) mRNA expression and pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) were measured using the quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) methods, respectively. AA-induced ulcerative colitis in rats was associated with edema and severe damage to the epithelium, infiltration of inflammatory cells, and the presence of ulcers in the colon tissue. The results showed that rats who were administered AA showed a decrease in the expression of HO-1, Nrf2, and NQO1 and increased protein levels of TNF-α and IL-1β than the control group. Rats were administered ferulic acid, quinic acid and, dexamethasone significantly improved histopathological indices. The expression of HO-1, Nrf2, and NQO1 were upregulated by 60 mg/kg of ferulic acid, 60 and100 mg/kg of quinic acid and, 2 mg/kg of dexamethasone treatment compared to the ulcerative colitis group. The protein levels of TNF-α and IL-1β dose-dependently decreased by ferulic acid and quinic acid treatment compared to the ulcerative colitis group. Ferulic acid and quinic acid effectively reduce inflammation and mucosal damage in rats with ulcerative colitis, especially when administered in high doses. The possible mechanism of anti-inflammatory response by ferulic acid and quinic acid may involve the activating of the Nrf2/HO-1 pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Nano Selenium on Cadmium Chloride-Induced Infertility in Male Wistar Rats","authors":"Shahrbano Taromsari,&nbsp;Akram Eidi,&nbsp;Pejman Mortazavi,&nbsp;Mehrdad Modaresi","doi":"10.1002/jbt.70179","DOIUrl":"https://doi.org/10.1002/jbt.70179","url":null,"abstract":"<div>\u0000 \u0000 <p>Selenium (Se) is an essential trace element with well-documented health benefits, including antioxidative, anti-inflammatory, antiapoptotic, and anticarcinogenic properties. Selenium nanoparticles (nano-Se) represent an advanced Se delivery system characterized by superior bioavailability and a reduced risk of Se-related toxicity. This study investigates the protective efficacy of nano-Se against cadmium chloride (CdCl₂)-induced infertility in adult male Wistar rats. The experimental design involved random allocation of the rats into nine groups: a healthy control group, a vehicle control group, three groups receiving nano-Se alone at 0.05, 0.1, and 0.2 mg/kg b.w./day, a group exposed to CdCl₂ to induce infertility, and three CdCl₂-exposed groups treated with nano-Se. After 30 days of treatment, the animals were euthanized for biochemical and histopathological assessments. The findings revealed that nano-Se administration ameliorated the detrimental effects of treatment CdCl₂ on serum testosterone levels. Additionally, nano-Se significantly reduced malondialdehyde levels and enhanced the activity of antioxidant enzymes in testicular homogenates. Histological analyses further demonstrated that nano-Se preserved the structural integrity of testicular tissue in the CdCl₂-induced fertility model. Nano-Se modulated apoptotic pathways, as evidenced by the suppression of Bax expression and upregulation of Bcl₂ expression in testicular tissue. Furthermore, nano-Se mitigated the overexpression of aquaporin-9 in CdCl₂-exposed rats. Collectively, these results provide robust biochemical, histological, and biochemical evidence supporting the potential therapeutic utility of nano-Se in mitigating testicular dysfunction.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal miR-107 Derived From Cigarette Smoking-Exposed Bronchial Epithelial Cells Aggravates Acute Lung Injury by Polarizing Macrophage to Proinflammatory Phenotype","authors":"Xin Ni,&nbsp;Yufeng Lv,&nbsp;Lei Han,&nbsp;Qian Wang,&nbsp;Jia Wang,&nbsp;Tongtong Liu,&nbsp;Li Zhang","doi":"10.1002/jbt.70139","DOIUrl":"https://doi.org/10.1002/jbt.70139","url":null,"abstract":"<div>\u0000 \u0000 <p>Exosomes are critical mediators of intercellular crosstalk and play significant roles in the progression of various diseases including acute lung injury (ALI). However, the specific role of exosomes in ALI remains largely unexplored. In investigation, we demonstrated that exosomes released from cigarette smoke extract (CSE)-exposed bronchial epithelial cells (BEAS-2B) facilitated M1 macrophage polarization. Notably, CSE exposure enhanced the production of miR-107 within these exosomes. Inhibition of miR-107 markedly reversed the M1 macrophage polarization and inflammatory responses in vitro and ameliorated lung injury in vivo. Furthermore, exosomal miR-107 was found to downregulate KLF4, thereby promoting M1 macrophage polarization and inflammation of macrophages. Collectively, these findings demonstrate that CSE-exposed BEAS-2B cells could induce M1 macrophage polarization via transmitting exosomal miR-107, and eventually ultimately contributing to the progression of ALI, indicating a potential therapeutic strategy for ALI.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-207 Suppresses the Progression of SiO2-Induced Pulmonary Fibrosis by Targeting Smad3 to Regulate the TGF-β1/Smad3 Signaling Pathway in C57BL/6 Mice","authors":"Jia-hui Zhao,&nbsp;Shuang Li,&nbsp;Shu-ling Du,&nbsp;Gui-zhi Han,&nbsp;Huan Li,&nbsp;Bo Shao,&nbsp;Xia Liu,&nbsp;Yuting Zhou,&nbsp;Zhao-qiang Zhang","doi":"10.1002/jbt.70170","DOIUrl":"https://doi.org/10.1002/jbt.70170","url":null,"abstract":"<div>\u0000 \u0000 <p>Silicosis is a worldwide occupational disease characterized by irreversible pulmonary fibrosis. Recent studies have showed that microRNAs (miRNAs) may play a crucial role in silicosis progression by modulating fibrosis-related gene express. In this study, we selected miR-207 as our research subject because we found that miR-207 can be match with Smad3 using bioinformatic techniques, which might silence the key fibrosis-related TGF-β1/Smad3 signal pathway. In this study, the mice were given silica suspension (20 µg/µL, 80 µL) via nostril once a day for 16 days to establish silicosis models, and then were transfected with miR-207 mimic or inhibitor. The mice which were given phosphate-buffered saline (PBS) (80 µL) via nostril were used as control. All mice were killed on Day 45 after the first exposure to dust, after which their lungs were removed for pathological observation and to measure the hydroxyproline content. Then, real-time polymerase chain reaction and Western blot analysis were applied to detect the relative expression levels of TGF-β1/Smad3 signaling pathway indicators (TGF-β1, TGF-βR, and Smad3), and myofibroblast transformation indicators (α-SMA and Fn). Results showed that the lung pathological images of silicosis model group mice showed significant fibrosis, and TGF-β1, TGF-βR, Smad3, α-SMA, and Fn were all highly upregulated compared with the control group mice. Intervention with miR-207 mimics significantly inhibited pulmonary fibrosis in silicosis mice by downregulation of TGF-β1/Smad3 and inhibiting of myofibroblast formation. Whereas these phenomena were not observed in silicosis mice treated with miR-207 inhibitor. The results demonstrated that miR-207 can block the progression of SiO₂-induced pulmonary fibrosis by targeting the TGF-β/Smad3 signaling pathway.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143404454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fenofibrate Reduces Ischemic Cerebral Edema via the Suppression of Aquaporin-4","authors":"Ming Zhou,&nbsp;Wei Zhao,&nbsp;Xinglong Qian","doi":"10.1002/jbt.70159","DOIUrl":"https://doi.org/10.1002/jbt.70159","url":null,"abstract":"<div>\u0000 \u0000 <p>The study aimed to investigate the neuroprotective effects of fenofibrate (FENO), a triglyceride-lowering drug, in rats with cerebral ischemia. An ischemic cerebral edema model was established in rats, and an oxygen–glucose deprivation/reoxygenation (OGD/R) model was created in astrocytes. Neurological deficits were quantified using a standardized deficit score. Protein expression levels were assessed through immunohistochemical staining, western blot analysis, and enzyme-linked immunosorbent assays (ELISA). Gene expression was determined using real-time polymerase chain reaction (RT-PCR), while luciferase activity was measured using a commercially available kit. We found that FENO significantly reduced infarct volume and neurological deficits in rats subjected to middle cerebral artery occlusion (MCAO). Additionally, FENO inhibited increased brain water content and upregulated the expression of aquaporin-4 (AQP4), a protein associated with cerebral edema, in the ischemic hemisphere. Furthermore, FENO suppressed the inflammatory response in cortical tissue by reducing the expression of cytokines such as interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α). It also increased the expression of myeloperoxidase (MPO) and promoted activation of astrocytes by increasing glial fibrillary acidic protein (GFAP). In vitro experiments further demonstrated that FENO reduced the expression of AQP4 against OGD/R in primary rat astrocytes. FENO also inhibited the activation of p38 by reducing its phosphorylation. Correspondingly, FENO suppressed the activation of activator protein 1 (AP-1) by reducing the levels of c-Jun and c-Fos, as well as the luciferase activity of AP-1. These effects were enhanced by the p38 specific inhibitor SB203580. Notably, the presence of the AP-1 specific inhibitor T5224 further promoted the effects of FENO in suppressing the expression of AQP4, implicating that the inhibitory effects of FENO on AQP4 expression are mediated by the p38/AP-1 signaling pathway. These findings suggest that FENO may have potential therapeutic benefits in stroke by targeting the p38/AP-1 signaling pathway and reducing AQP4 expression, thereby alleviating cerebral edema and inflammation.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unlocking Naringin's Potential: A Systematic Review and Meta-Analysis of Its Nephroprotective Effects in Pre-Clinical Models","authors":"Akanksh Das,&nbsp;Vibhu Bhardwaj,&nbsp;Gollapalle Lakshminarayanashastry Viswanatha,&nbsp;Hanumanthappa Shylaja,&nbsp;Hemavathi Gajendra,&nbsp;Ch K V L S N Anjana Male","doi":"10.1002/jbt.70149","DOIUrl":"https://doi.org/10.1002/jbt.70149","url":null,"abstract":"<div>\u0000 \u0000 <p>This systematic review and meta-analysis aimed to evaluate and summarize the therapeutic effects of naringin on various kidney diseases, based on preclinical research. A comprehensive literature search was performed using electronic databases such as PubMed/Medline and Google Scholar, concentrating on the impact of naringin in different experimental animal models of kidney disease. After applying the inclusion and exclusion criteria, 27 studies were chosen for analysis. The meta-analysis revealed that naringin treatment significantly improved body weight gain and markers of kidney function, as evidenced by decreased serum urea, creatinine, and blood urea nitrogen (BUN) levels. Additionally, naringin treatment normalized antioxidant parameters, restored enzymes like superoxide dismutase and catalase, and alleviated oxidative stress markers, comprising myeloperoxidase and reactive oxygen species. Besides, naringin also alleviated inflammation as indicated by reduced levels of markers such as NF-κB, IL-6, KIM-1, COX-2, and TNF-α. Furthermore, it regulated apoptosis by decreasing the Bax, caspase-3, and p53 levels while increasing Bcl-2. In summary, the meta-analysis demonstrated that naringin significantly mitigates nephrotoxicity induced by oxidative stress, chemotherapy, drugs, and chemicals. This nephroprotective effect is mediated through a combination of several mechanisms, including antioxidant, anti-inflammatory, and anti-apoptotic pathways. These cellular and molecular improvements were associated with enhanced kidney structure, function, and overall physiology following naringin treatment. Overall, this systematic review and meta-analysis provide strong scientific evidence supporting the therapeutic potential of naringin in managing kidney diseases.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL3-mediated NFAT5 Upregulation Promotes Cervical Cancer Progression Through Enhancing the Mitochondrial Function by Transcriptional Regulation of PRDX1","authors":"Yanli He,&nbsp;Junli Ge,&nbsp;Shuhua Zhao,&nbsp;Fuxing Zhou,&nbsp;Wei Zou,&nbsp;Yan Gao,&nbsp;Shujuan Liu,&nbsp;Wei Zhang","doi":"10.1002/jbt.70162","DOIUrl":"https://doi.org/10.1002/jbt.70162","url":null,"abstract":"<div>\u0000 \u0000 <p>Nuclear factor of activated T-cells 5 (NFAT5) is recognized as an oncogene in a variety of tumors. However, the role of NFAT5 in cervical cancer (CC) cell phenotypic alterations remains to be elucidated. Here, we demonstrated that NFAT5 expression was elevated in CC samples and cells using quantitative real-time reverse transcription PCR, Western blot analysis, and immunohistochemistry assays, and high NFAT5 expression showed a poor prognosis. After C-33A cells were transfected with pcDNA-NFAT5 or NFAT5-short hairpin RNA (shRNA), cell proliferation, invasion, and apoptosis were evaluated using CCK-8 and EdU assays, transwell assays, and flow cytometry, respectively. Biomarkers indicating mitochondrial function, including the expression of the <span>d</span>-loop, ATP levels, and mitochondrial membrane potential, were detected. NFAT5 knockdown restrained cell proliferation and invasion, impaired mitochondrial function, and increased the ratio of cell apoptosis; however, NFAT5 overexpression showed the opposite results. RNA immunoprecipitation (RIP) and methylated RIP (MeRIP) assays were performed to identify interactions among NFAT5, methyltransferase-like 3 (METTL3), and insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3). Chromatin immunoprecipitation and dual-luciferase reporter gene assays demonstrated that NFAT5 binds to the peroxiredoxin 1 (PRDX1) promoter to drive PRDX1 transcription. METTL3 enhanced NFAT5 mRNA stability through IGF2BP3-mediated N6-Methyladenosine (m⁶A) modification, and NFAT5 transcriptionally regulated PRDX1 expression. Moreover, the reintroduction of METTL3 or PRDX1 promoted cell growth and mitochondrial function damage in NFAT5-silenced cells. In vivo experiments further demonstrated that NFAT5 promotes CC tumor growth. Taken together, NFAT5 upregulation mediated by the METTL3/IGF2BP3 complex in an m⁶A-dependent manner facilitates CC cell growth by transcriptionally regulating PRDX1 expression, providing a novel target for CC therapy.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of Postoperative Cognitive Dysfunction by Glutathione Under Various Pathways: A Narrative Review","authors":"Yan Lin He,&nbsp;Ying Zhang,&nbsp;Qing Liu","doi":"10.1002/jbt.70154","DOIUrl":"https://doi.org/10.1002/jbt.70154","url":null,"abstract":"<div>\u0000 \u0000 <p>Postoperative cognitive dysfunction (POCD) is a common neurological complication after surgery and general anesthesia, and the incidence increases with age. Will have a negative impact on patients, family and society. At present, neuroinflammation and oxidative stress are the main recognized mechanisms. Glutathione (GSH) is a powerful reducing agent and may be related to POCD. Data Collection: Using medical search engines such as PubMed, Web of Science, we analyzed articles on topics such as: POCD, GSH, microglia, astrocyte, oligodendrocyte, ferroptosis, BDNF, Neuroinflammation, oxidative stress. The above topics are searched in databases using Boolean operations. We included original articles, reviews and other article types such as medical books. Results: According to the reviewed literature, GSH may be a treatment for POCD. Conclusions: Specific and targeted therapies for POCD still sparse, therefore, the implementation of preventive strategies appears to remain the optimal attitude. Further research is needed for a better understanding of GSH and POCD.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review on miRNAs in Enteric Bacteria-mediated Host Pathophysiology: Mechanisms and Implications","authors":"Ahmed S. Doghish,&nbsp;Ola Elazazy,&nbsp;Hend H. Mohamed,&nbsp;Reda M. Mansour,&nbsp;Aml Ghanem,&nbsp;Ahmed H. I. Faraag,&nbsp;Mohammed S. Elballal,&nbsp;Mahmoud A. Elrebehy,&nbsp;Ahmed E. Elesawy,&nbsp;Sherif S. Abdel Mageed,&nbsp;Sameh Saber,&nbsp;Yara A. Nassar,&nbsp;Ahmed I. Abulsoud,&nbsp;Mustafa Ahmed Abdel-Reheim,&nbsp;Alaa S. Elawady,&nbsp;Mohamed A. Ali,&nbsp;Mohamed Salah Basiouny,&nbsp;Mohamed Hemdan,&nbsp;Radwa H. Lutfy,&nbsp;Farah A. Awad,&nbsp;Salma A. El-Sayed,&nbsp;Mohamed M. Ashour,&nbsp;Gharieb S. El-Sayyad,&nbsp;Osama A. Mohammed","doi":"10.1002/jbt.70160","DOIUrl":"10.1002/jbt.70160","url":null,"abstract":"<div>\u0000 \u0000 <p>Recently, many studies focused on the billions of native bacteria found inside and all over the human body, commonly known as the microbiota, and its interactions with the eukaryotic host. One of the niches for such microbiota is the gastrointestinal tract (GIT), which harbors hundreds to thousands of bacterial species commonly known as enteric bacteria. Changes in the enteric bacterial populations were linked to various pathologies such as irritable bowel syndrome and obesity. The gut microbiome could affect the health status of individuals. MicroRNAs (miRNAs) are one of the extensively studied small-sized noncoding RNAs (ncRNAs) over the past decade to explore their multiple roles in health and disease. It was proven that miRNAs circulate in almost all body fluids and tissues, showing signature patterns of dysregulation associated with pathologies. Both cellular and circulating miRNAs participate in the posttranscriptional regulation of genes and are considered the potential key regulators of genes and participate in cellular communication. This manuscript explores the unique interplay between miRNAs and enteric bacteria in the gastrointestinal tract, emphasizing their dual role in shaping host-microbiota dynamics. It delves into the molecular mechanisms by which miRNAs influence bacterial colonization and host immune responses, linking these findings to gut-related diseases. The review highlights innovative therapeutic and diagnostic opportunities, offering insights for targeted treatments of dysbiosis-associated pathologies.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KDM1A Acts as an Oncogene and Facilitates the Epithelial Mesenchymal Transition Process in Gastric Cancer","authors":"Rongjie Huang,&nbsp;Yichen Cai,&nbsp;Qiuxian Chen,&nbsp;Yuqin Sun,&nbsp;Mingqiao Lian,&nbsp;Mingjie Lian,&nbsp;Lisheng Cai","doi":"10.1002/jbt.70120","DOIUrl":"10.1002/jbt.70120","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>This study is performed to research the biological role of KDM1A in the epithelial mesenchymal transition (EMT) of gastric cancer and investigate the mechanism involved.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The KDM1A, Vimentin and E-cadherin levels were studied, as well as the correlation among them in gastric cancer samples. Gastric cancer cells were transfected with KDM1A overexpression and knockdown, and the cellular infiltration, motility, morphology and F-actin expression were subsequently identified. For the protein level assessment of EMT, the western blot analysis combined with immunofluorescence was employed. The effect of KDM1A on TGF-β/Notch signaling was also detected.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>KDM1A was overexpressed in gastric cancer tumor tissues. In the clinical gastric carcinoma samples, the level of KDM1A was linked negatively to the expression of E-cadherin, while positively to the expression of Vimentin. Among the gastric carcinoma population, the expression of KDM1A was linked to the lymph node metastasis, TNM stage and tumor differentiation. The KDM1A downregulation prohibited the cellular motility, infiltration and F-actin expression, and suppressed EMT process. KDM1A overexpression exhibited promoting effect on EMT in gastric cancer cells. KDM1A regulated TGF-β/Notch signaling to affect EMT in gastric cancer cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>KDM1A acts as an oncogene and facilitates the epithelial mesenchymal transition process by regulating TGF-β/Notch signal pathway in gastric cancer cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}