Journal of Biochemical and Molecular Toxicology最新文献_第4页

Let-7 reduces the proliferation and migration of oral cancer cells via PI3K/AKT signaling pathway Let-7 可通过 PI3K/AKT 信号通路减少口腔癌细胞的增殖和迁移。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-09-04 DOI: 10.1002/jbt.23834

Yang Liu, Kunshan Li, Jing Zhang, Linyu Jin, Hui Xu, Yanhao Duan

{"title":"Let-7 reduces the proliferation and migration of oral cancer cells via PI3K/AKT signaling pathway","authors":"Yang Liu, Kunshan Li, Jing Zhang, Linyu Jin, Hui Xu, Yanhao Duan","doi":"10.1002/jbt.23834","DOIUrl":"10.1002/jbt.23834","url":null,"abstract":"The involvement of let-7 in the occurrence and progression of various cancers has been well-documented. However, the precise molecular mechanisms underlying its impact on oral cancer development remain unclear. In this study, we aimed to elucidate the role of let-7 in oral cancer progression and investigate its underlying molecular mechanisms. The expression of let-7 and high mobility group A2 (HMGA2) mRNA was assessed using the quantitative reverse transcription polymerase chain reaction. Western blot analysis was employed to detect the expression of key proteins in the PI3K/AKT signaling pathway as well as HMGA2 protein levels. The targeting relationship between let-7 and HMGA2 was predicted through bioinformatics methods and confirmed via luciferase reporter gene assay. The effects of let-7 and HMGA2 on the functionality of oral cancer cells were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, colony formation assay, Transwell assay, wound healing assay, and Annexin V/PI apoptosis assay. Additionally, the impact of let-7 on the growth of oral cancer cells in vivo was investigated by inducing subcutaneous tumor formation in nude mice. Let-7 effectively suppresses the proliferation, migration, and invasion of oral cancer cells by inhibiting the activation of the PI3K/AKT signaling pathway. HMGA2, a downstream target gene of let-7, exhibits high expression in oral cancer. However, overexpression of HMGA2 diminishes the inhibitory effects induced by let-7 overexpression on the proliferation, migration, and invasion of oral cancer cells. The occurrence and progression of oral cancer cells are inhibited by Let-7 through the downregulation of HMGA2, potentially mediated by the inhibition of PI3K/AKT signaling pathway activation.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125813","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}

引用次数: 0

RETRACTION: Preventive Effect of Naringin on Cardiac Mitochondrial Enzymes During Isoproterenol-induced Myocardial Infarction in Rats: A Transmission Electron Microscopic Study 返回：柚皮苷对异丙肾上腺素诱发大鼠心肌梗死期间心脏线粒体酶的预防作用：透射电子显微镜研究。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-09-04 DOI: 10.1002/jbt.23839

引用次数: 0

Melatonin alleviates arsenic-induced liver injury by regulating protein RKIP and enhancing antioxidant defencse mechanisms 褪黑素通过调节蛋白 RKIP 和增强抗氧化防御机制减轻砷诱发的肝损伤

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-31 DOI: 10.1002/jbt.23835

Soheil Rezvankhah, Felor Zargari, Rasoul Sharifi

{"title":"Melatonin alleviates arsenic-induced liver injury by regulating protein RKIP and enhancing antioxidant defencse mechanisms","authors":"Soheil Rezvankhah, Felor Zargari, Rasoul Sharifi","doi":"10.1002/jbt.23835","DOIUrl":"https://doi.org/10.1002/jbt.23835","url":null,"abstract":"Arsenic (As) is a highly toxic metal and one of the main factors in cancer development through oxidative stress and production of reactive oxygen species. Prior research has demonstrated melatonin's potential as a free radical scavenger. Raf kinase inhibitory protein (RKIP) is an important regulator of intracellular signaling pathways that has been linked to various types of cancer. The aim of this research was to explore the influence of melatonin's antioxidant properties on the expression of the protein RKIP and the antioxidant status of liver tissue in rats that were exposed to arsenic. Thirty two male Wistar rats were divided into four groups of eight, including control, melatonin-treated (20 mg/Kg of melatonin), sodium arsenite-treated (5.5 mg/Kg of sodium arsenite), and melatonin + sodium arsenite-treated groups (combination) for 4 weeks. The expression level of protein RKIP was measured by Western blot, and malondialdehyde (MDA) content of the liver as well as the activities of antioxidant enzymes were measured. The data analyzed using one-way ANOVA (significance level of p < 0.05) and GraphPad Prism (9) software. Sodium arsenite treatment led to a significant decrease in RKIP protein expression and antioxidant enzyme activity, and an increase in liver MDA levels (p < 0.001). Conversely, melatonin treatment in the combination group resulted in a significant increase in RKIP protein expression and antioxidant enzyme activity and a decrease in liver MDA levels (p < 0.05). These findings suggest that melatonin can attenuate oxidative damage caused by arsenic in liver cells by enhancing RKIP protein expression and antioxidant enzyme activity.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100377","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}

引用次数: 0

Silencing of KIAA1429, a N6-methyladenine methyltransferase, inhibits the progression of colon adenocarcinoma via blocking the hypoxia-inducible factor 1 signalling pathway 抑制 N6-甲基腺嘌呤甲基转移酶 KIAA1429 可通过阻断缺氧诱导因子 1 信号通路抑制结肠腺癌的发展

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-31 DOI: 10.1002/jbt.23829

Canhui Ouyang, Guofeng Xu, Jun Xie, Yun Xie, Yun Zhou

{"title":"Silencing of KIAA1429, a N6-methyladenine methyltransferase, inhibits the progression of colon adenocarcinoma via blocking the hypoxia-inducible factor 1 signalling pathway","authors":"Canhui Ouyang, Guofeng Xu, Jun Xie, Yun Xie, Yun Zhou","doi":"10.1002/jbt.23829","DOIUrl":"https://doi.org/10.1002/jbt.23829","url":null,"abstract":"KIAA1429 is an important ‘writer’ of the N6-methyladenine (m6A) modification, which is involved in tumour progression. This study was conducted to explore the mechanism of action of KIAA1429 in colon adenocarcinoma (COAD). KIAA1429-silenced COAD cell and xenograft tumour models were constructed, and the function of KIAA1429 was explored through a series of in vivo and in vitro assays. The downstream mechanisms of KIAA1429 were explored using transcriptome sequencing. Dimethyloxalylglycine (DMOG), an activator of HIF-1α, was used for feedback verification. The expression of KIAA1429 in COAD tumour tissues and cells was elevated, and KIAA1429 exhibited differential expression at different stages of the tumour. Silencing of KIAA1429 inhibited the proliferation, migration, and invasion of HT29 and HCT116 cells. The expression levels of NLRP3, GSDMD and Caspase-1 were decreased in KIAA1429-silenced HT29 cells, indicating the pyroptotic activity was inhibited. Additionally, KIAA1429 silencing inhibited the growth of tumour xenograft. Transcriptome sequencing and reverse transcription quantitative polymerase chain reaction revealed that after KIAA1429 silencing, the expression of AKR1C1, AKR1C2, AKR1C3 and RDH8 was elevated, and the expression of VIRMA, GINS1, VBP1 and ARF3 was decreased. In HT29 cells, KIAA1429 silencing blocked the HIF-1 signalling pathway, accompanied by the decrease in AKT1 and HIF-1α protein levels. The activation of HIF-1 signalling pathway, mediated by DMOG, reversed the antitumour role of KIAA1429 silencing. KIAA1429 silencing inhibits COAD development by blocking the HIF-1 signalling pathway.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100293","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}

引用次数: 0

Unveiling the antibacterial efficacy of thiazolo [3,2-a] pyrimidine: Synthesis, molecular docking, and molecular dynamic simulation 揭示噻唑并[3,2-a]嘧啶的抗菌功效：合成、分子对接和分子动力学模拟

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-31 DOI: 10.1002/jbt.23822

Vishant C. Patel, Ankit J. Patel, Darshan S. Patel, Amit B. Dholakia, Siddique Akber Ansari, Mohit Agrawal

{"title":"Unveiling the antibacterial efficacy of thiazolo [3,2-a] pyrimidine: Synthesis, molecular docking, and molecular dynamic simulation","authors":"Vishant C. Patel, Ankit J. Patel, Darshan S. Patel, Amit B. Dholakia, Siddique Akber Ansari, Mohit Agrawal","doi":"10.1002/jbt.23822","DOIUrl":"https://doi.org/10.1002/jbt.23822","url":null,"abstract":"Two series of C-Mannich base derivatives were synthesized and evaluated through the reaction of formaldehyde, two thiazolo-pyrimidine compounds, and various 2°-amines. The chemical structures and inherent properties of the synthesized compounds were authenticated using a variety of spectroscopic techniques. The aseptic bactericidal potential of the compounds was assessed alongside five common bacterial microbes, with Ampicillin employed as the reference drug. Compounds 9b and 9d demonstrated comparable antibacterial activity to ampicillin against Bacillus subtilis and Bacillus megaterium, respectively, at 100 μg/mL. Furthermore, compounds 9f and 10f exhibited noteworthy action against Staphylococcus aureus (MIC: 250 μg/mL). Compounds 10b and 10f displayed excellent efficacy versus Escherichia coli, boasting (MIC: 50 μg/mL). Molecular docking studies elucidated the necessary connections and energies of molecular entities with the E. coli DNA gyrase B enzyme, a pivotal target in bacterial DNA replication. Further thermodynamic stability of the ligand-receptor complex of 10b and 10f were further validated though 200 ns molecular dynamics simulation. The findings highlight the potential of these synthesized derivatives as effective antibacterial agents and provide valuable insights into their mechanism of action.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100376","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}

引用次数: 0

CircETV6 acts as an oncogenic driver in hepatocellular carcinoma progression CircETV6 是肝细胞癌发展过程中的致癌驱动因子

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-31 DOI: 10.1002/jbt.23766

Xiaoqin Li, Xuemei Jiang, Jing Lu, Lan Jiang, Yan Li, Yuting Lin, Feng Wan, Changmin Wang

{"title":"CircETV6 acts as an oncogenic driver in hepatocellular carcinoma progression","authors":"Xiaoqin Li, Xuemei Jiang, Jing Lu, Lan Jiang, Yan Li, Yuting Lin, Feng Wan, Changmin Wang","doi":"10.1002/jbt.23766","DOIUrl":"https://doi.org/10.1002/jbt.23766","url":null,"abstract":"Circular RNA (circRNA) plays important role in hepatocellular carcinoma (HCC) progression. However, the role and mechanism of circETV6 in HCC progression remain unclear. The levels of circETV6, ETV6, miR-383-5p, and PTPRE were tested by quantitative reverse-transcription polymerase chain reaction. Cell functions were assessed using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay, 5-ethynyl-2′-deoxyuridine assay, colony formation assay, wound healing assay, transwell assay, and flow cytometry. The protein levels of poptosis-related markers and PTPRE were determined by western blot analysis. RNA interaction was analyzed by dual-luciferase reporter assay and RNA pull-down assay. A xenograft model was established to assess circETV6 roles in vivo. CircETV6 was highly expressed in HCC tissues and cells. CircETV6 knockdown repressed HCC cell proliferation, migration, invasion, and cell cycle, while accelerated apoptosis. CircETV6 targeted miR-383-5p, and miR-383-5p inhibition reversed the regulation of circETV6 knockdown on HCC cell progression. CircETV6 promoted PTPRE level via targeting miR-383-5p. Overexpressed PTPRE abolished the inhibition effect of miR-383-5p on HCC cell progression. In addition, circETV6 knockdown slowed HCC tumor growth in vivo. CircETV6 might facilitate HCC progression via the miR-383-5p/PTPRE axis, providing a novel target for HCC treatment.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100291","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}

引用次数: 0

Expression of Concern: Naringin prevents Ultraviolet-B radiation-induced oxidative damage and inflammation through activation of peroxisome proliferator-activated receptor γ in mouse embryonic fibroblast (NIH-3T3) cells 表达关注：柚皮苷通过激活小鼠胚胎成纤维细胞（NIH-3T3）中的过氧化物酶体增殖激活受体γ，防止紫外线-B 辐射诱导的氧化损伤和炎症反应

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-31 DOI: 10.1002/jbt.23840

{"title":"Expression of Concern: Naringin prevents Ultraviolet-B radiation-induced oxidative damage and inflammation through activation of peroxisome proliferator-activated receptor γ in mouse embryonic fibroblast (NIH-3T3) cells","authors":"","doi":"10.1002/jbt.23840","DOIUrl":"https://doi.org/10.1002/jbt.23840","url":null,"abstract":"R. NilamberLal Das, S. Muruhan, R. P. Nagarajan and A. Balupillai, “Naringin Prevents Ultraviolet-B Radiation-induced Oxidative Damage and Inflammation Through Activation of Peroxisome Proliferator-activated Receptor γ in Mouse Embryonic Fibroblast (NIH-3T3) Cells,” Journal of Biochemical and Molecular Toxicology 33, no. 3 (2019): e22263, https://doi.org/10.1002/jbt.22263.This Expression of Concern for the above article published online on 4 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been published by agreement between the journal Editor-in-Chief, Hari K. Bhat; and Wiley Periodicals, Inc. The Expression of Concern has been agreed following concerns raised by a third party regarding the standard deviations presented in Table 2, which are unusually low and show an unexpected even distribution. The authors admitted they made a mistake and wished to correct Table 2. However, since the new data provided could not be substantiated, the editors did not consider the data appropriate to correct the article. The editors would like to issue an Expression of Concern to alert the readers.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jbt.23840","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to “MicroRNA-505-3p mediates cell motility of epithelial ovarian cancer via suppressing PEAK1 expression” 对 "MicroRNA-505-3p 通过抑制 PEAK1 的表达介导上皮性卵巢癌的细胞运动 "的更正

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-31 DOI: 10.1002/jbt.23828

引用次数: 0

Cordycepin ameliorates kidney injury by inhibiting gasdermin D-mediated pyroptosis of renal macrophages through nuclear factor kappa-B 虫草素通过核因子卡巴-B抑制气敏素 D 介导的肾巨噬细胞热凋亡，从而改善肾损伤

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-29 DOI: 10.1002/jbt.23824

Zhiling Tang, Yu Zhu

{"title":"Cordycepin ameliorates kidney injury by inhibiting gasdermin D-mediated pyroptosis of renal macrophages through nuclear factor kappa-B","authors":"Zhiling Tang, Yu Zhu","doi":"10.1002/jbt.23824","DOIUrl":"https://doi.org/10.1002/jbt.23824","url":null,"abstract":"To explain the effect and mechanism of cordycepin (COR) in resisting acute kidney injury (AKI). Network pharmacology was employed to analyze the correlations between COR, AKI, and pyroptosis, as well as the action target of COR. A mouse model of AKI was established by ischemia reperfusion injury (IRI), and after treatment with COR, the renal function, tissue inflammatory cytokine levels, and pyroptosis-related signals were detected in mice. In in-vitro experiments, damage of renal macrophages was caused by the oxygen-glucose deprivation model, and pyroptosis indicators and inflammatory cytokine levels were assayed after COR treatment. Network pharmacological analysis revealed that nuclear factor kappa-B (NF-κB) was the primary action target of COR and that COR could inhibit kidney injury and tissue inflammation during IRI by inhibiting NF-κB-mediated gasdermin D cleavage. When NF-κB was inhibited, the effect of COR was weakened. COR in renal macrophages could inhibit pyroptosis and lower the levels of inflammatory cytokines, whose effect was associated with NF-κB. Our study finds that COR can play an anti-inflammatory role and inhibit the progression of AKI through the NF-κB-mediated pyroptosis, which represents its nephroprotective mechanism.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142099954","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}

引用次数: 0

Ginsenoside RD prevents acute liver injury in mice by inhibiting STAT3-mediated NLRP3/GSDMD activation 人参皂苷 RD 通过抑制 STAT3 介导的 NLRP3/GSDMD 激活，预防小鼠急性肝损伤。

IF 3.2 3区医学

Journal of Biochemical and Molecular Toxicology Pub Date : 2024-08-28 DOI: 10.1002/jbt.23825

Wenyan Li, Yun Kong, Caiqun Zhang

{"title":"Ginsenoside RD prevents acute liver injury in mice by inhibiting STAT3-mediated NLRP3/GSDMD activation","authors":"Wenyan Li, Yun Kong, Caiqun Zhang","doi":"10.1002/jbt.23825","DOIUrl":"10.1002/jbt.23825","url":null,"abstract":"We investigated the role and mechanism of ginsenoside RD (GRD) in acute liver injury. Network pharmacology was used to analyze the correlations among GRD-liver injury-pyroptosis targets. A mouse model of acute liver injury was established by lipopolysaccharide + d-galactose（LPS + d/Gal). After pretreatment with GRD, the changes in mouse liver function were detected. The histopathological changes were assayed by hematoxylin and eosin and Masson staining, the tissue expressions of inflammatory cytokines were detected by enzyme-linked immunosorbent assay, and the protein expressions were assayed by immunohistochemical staining and Western blotting. Meanwhile, mechanism research was conducted using STAT3-knockout transgenic mice and STAT3-IN13, a STAT3 inhibitor. GRD inhibited liver injury, mitigated tissue inflammation, and suppressed STAT3-mediated pyroptosis in mice. After applying STAT3-knockout mouse model or STAT3-IN13, GRD did not further inhibit the liver injury. GRD can resist liver injury by inhibiting the STAT3-mediated pyroptosis, which is one of the hepatoprotective mechanisms of GRD.","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080399","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}

引用次数: 0