Environmental Toxicology最新文献_第3页

RETRACTION: Circular Forms of Dedicator of Cytokinesis 1 Promotes Breast Cancer Progression by Derepressing Never in Mitosis Related Kinase 2 via Sponging miR-128-3p. 回放：细胞分裂驱动因子 1 的环状形式通过海绵状 miR-128-3p 解除对有丝分裂相关激酶 2 的抑制，从而促进乳腺癌的进展。

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-25 DOI: 10.1002/tox.24448

引用次数: 0

Aglaia elliptifolia Leaf Extract Inhibits Autophagy‐Related 4B Protease and Suppresses Malignancies of Colorectal Cancer Cells 椭圆木叶提取物能抑制自噬相关 4B 蛋白酶并抑制结直肠癌细胞恶变

IF 4.5 3区医学

Environmental Toxicology Pub Date : 2024-11-23 DOI: 10.1002/tox.24439

Jing‐Ru Weng, Chih‐Wen Shu, Chia‐Che Chang, Ya‐Chun Wu, Hsiu‐Chen Yang, Cheng‐Hsin Lee, Hans‐Uwe Dahms, Wei‐Yu Lin, Chun‐Lin Chen, Pei‐Feng Liu

{"title":"Aglaia elliptifolia Leaf Extract Inhibits Autophagy‐Related 4B Protease and Suppresses Malignancies of Colorectal Cancer Cells","authors":"Jing‐Ru Weng, Chih‐Wen Shu, Chia‐Che Chang, Ya‐Chun Wu, Hsiu‐Chen Yang, Cheng‐Hsin Lee, Hans‐Uwe Dahms, Wei‐Yu Lin, Chun‐Lin Chen, Pei‐Feng Liu","doi":"10.1002/tox.24439","DOIUrl":"https://doi.org/10.1002/tox.24439","url":null,"abstract":"Autophagy is a self‐eating pathway for maintaining normal cellular physiology, while dysregulation of autophagy is associated with cancer progression. Autophagy‐related 4B gene (ATG4B) is a cysteine protease to regulate autophagosome formation and is positively correlated with poor prognosis of colorectal cancer (CRC) patients. An increasing number of reports have implied that ATG4B might be an attractive drug target for CRC. Natural products are the most important source of drug development for cancer therapy due to their high degree of diversity in chemical structure. However, there are few natural products targeting autophagy regulation, especially targeting ATG4B. We aim to identify effective natural compounds from costal plants against ATG4B as potential CRC therapies. We extracted the whole plants, stem, and leaves from nine coastal plant species of Taiwan using different solvents including acetone, methanol, or chloroform. We then evaluated their effects on ATG4B activity and cancer malignancy in CRC cells (DLD‐1, HCT116, and SW620). Among these 26 extracts, we found that the methanol leaf extract of A. elliptifolia significantly inhibited ATG4B proteolytic activity. Moreover, cell viability and colony formation and mobility were decreased in CRC cells treated with the extract. The extract further reduced the number of living cells and induced subG1 proportion of CRC cells. The cytotoxicity of A. elliptifolia leaf extract was also enhanced in CRC cells under starvation, whereas it had no additional effects in ATG4B or autophagy deficient cells. Taken together, the methanol leaf extract of A. elliptifolia might contains bioactive compounds for inhibiting ATG4B and autophagy activity to diminish viability and mobility of CRC cells, indicating its potential as an anti‐CRC drug for future development.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"12 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142690746","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

Clothianidin Exposure Induces Cell Apoptosis via Mitochondrial Oxidative Damage. 氯噻酮暴露通过线粒体氧化损伤诱导细胞凋亡

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-22 DOI: 10.1002/tox.24442

Wei-Long Cheng, Zhi-Hui Zhang, Zhi-Bin Zhang, Guo-Ping Zhao, Yan-Bo Wang

{"title":"Clothianidin Exposure Induces Cell Apoptosis via Mitochondrial Oxidative Damage.","authors":"Wei-Long Cheng, Zhi-Hui Zhang, Zhi-Bin Zhang, Guo-Ping Zhao, Yan-Bo Wang","doi":"10.1002/tox.24442","DOIUrl":"https://doi.org/10.1002/tox.24442","url":null,"abstract":"Clothianidin (CLO) is a high-frequently detected neonicotinoid pesticide in fruits and vegetables, whose exposure security deserves attention. This study evaluated the apoptotic toxicity of CLO on Caco-2 cells at doses of 100 nM, 10 μM, and 1 mM. After exposure, CLO induced to a remarkable change of signaling proteins that participated in the process of cell apoptosis, including caspase 3, cleaved-caspase 3, and caspase 9. CLO treatment further induced a decrease of mitochondrial membrane potential and increased the protein level of cytochrome C. Reactive oxygen species (ROS) and intracellular Ca2+ were also found elevated, indicating an oxidative damage caused by CLO treatment. Moreover, the production of ROS occurred in advance of Ca2+ elevation, since inhibiting ROS production could recover the elevation of Ca2+ induced by CLO exposure. The protein level of metabolic enzyme cytochrome P450 3A4 (CYP3A4) was downregulated after the treatment of CLO. Molecular docking simulation indicated that CLO had good binding characteristics with CYP3A4. Amino acid sites Arg105, Arg130, and Leu373 in CYP3A4, and nitro group and chlorothiazole group in CLO structure might be the potential binding action target. These results indicated that CLO exposure could induce an apoptotic effect on Caco-2 cells, possibly acting through combining and inhibiting its metabolic enzyme CYP3A4, and then leading to oxidative stress and mitochondrial damage. Thus, CLO exposure might be a potential risk factor for human intestinal health.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692821","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

Bisphenol B Exposure Promotes Melanoma Progression via Dysregulation of Lipid Metabolism in C57BL/6J Mice. 双酚 B 暴露通过调节 C57BL/6J 小鼠的脂质代谢促进黑色素瘤的发展

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-22 DOI: 10.1002/tox.24441

Xuening Ma, Qianchao Shao, Shuxian Huang, Weigao Zhang, Hu Liu, Xu Jiayi, Xunan Zhao, Peiqi Li, Da Shao, YuanQing Bu, Dan Weng

{"title":"Bisphenol B Exposure Promotes Melanoma Progression via Dysregulation of Lipid Metabolism in C57BL/6J Mice.","authors":"Xuening Ma, Qianchao Shao, Shuxian Huang, Weigao Zhang, Hu Liu, Xu Jiayi, Xunan Zhao, Peiqi Li, Da Shao, YuanQing Bu, Dan Weng","doi":"10.1002/tox.24441","DOIUrl":"https://doi.org/10.1002/tox.24441","url":null,"abstract":"The increasing incidence of cancer underscore the necessity of investigating contributors such as endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA). Although BPA's risks are well-documented, comprehensive studies on its substitutes, such as bisphenol B (BPB), are limited. Dysregulated lipid metabolism is a hallmark of cancer progression. Our previous work demonstrated that BPA and bisphenol S (BPS) disrupt lipid metabolism via the peroxisome proliferator-activated receptor γ (PPARγ) pathway. We hence hypothesized that BPB might similarly perturb lipid metabolism and promote tumor growth. BPB's impact on lipid metabolism was investigated in vitro and in vivo using B16 melanoma cancer cells. Our findings indicate BPB exposure significantly increased lipid metabolism in B16 cells, enhancing cell proliferation and migration, and promoting tumor development in mice. Utilizing siRNA transfection or chemical inhibitor, we found that stearoyl-CoA desaturase-1 (SCD1), a key enzyme in lipid synthesis pathway, was required for BPB-induced lipid accumulation and cancer cell migration. Docking analysis revealed BPB may activate gene expression related to lipid metabolism and angiogenesis by interacting with PPARγ and hypoxia-inducible factor-1α (HIF-1α). This study illuminates BPB's potential role in advancing melanoma through lipid metabolism manipulation, highlighting the need for further research into the safety of BPA substitutes and their impact on cancer development.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686433","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

Chronic Exposure of Zebrafish to Iron and Aluminum: Evaluation of Reversal and Generational Transposition of Behavioral, Histopathological, and Genotoxic Changes. 斑马鱼与铁和铝的慢性接触：评估行为、组织病理学和遗传毒性变化的逆转和世代交替。

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-22 DOI: 10.1002/tox.24443

Gabriela Zimmermann Prado Rodrigues, Mariana Finkler, Thainá Garbino Dos Santos, Juliana Machado Kayser, Diego Del Duca Lima, Jorge Henrique Burghausen, Diogo Losch de Oliveira, Ana Luiza Ziulkoski, Günther Gehlen

{"title":"Chronic Exposure of Zebrafish to Iron and Aluminum: Evaluation of Reversal and Generational Transposition of Behavioral, Histopathological, and Genotoxic Changes.","authors":"Gabriela Zimmermann Prado Rodrigues, Mariana Finkler, Thainá Garbino Dos Santos, Juliana Machado Kayser, Diego Del Duca Lima, Jorge Henrique Burghausen, Diogo Losch de Oliveira, Ana Luiza Ziulkoski, Günther Gehlen","doi":"10.1002/tox.24443","DOIUrl":"https://doi.org/10.1002/tox.24443","url":null,"abstract":"This study aimed to report the effects of chronic exposure of zebrafish exposed to environmentally relevant concentrations of 0.5, 2.4, and 5.0 mg L-1 iron (Fe) and 0.2, 0.4, and 2.0 mg L-1 aluminum (Al). We also evaluated the reversal and generational transposition (F1) of possible histopathological, behavioral, and genotoxic changes in the species. Locomotion changes that may have been caused by the increase in the number of apoptotic cells and in the telencephalic mitochondrial activity were observed especially after the 30 days exposure to Al and persisted after recovery (30 days). We also observed histopathological changes, such as an increase in the number of intestinal goblet cells, even after the recovery period in these animals. Our results also showed that the Fe concentrations used were insufficient to cause genotoxicity, behavioral and intestinal epithelium changes. The adult offspring (F1) of animals exposed to Al showed changes in locomotion and in the amount of goblet cells, demonstrating that even in low concentrations this pollutant can harm subsequent generations in the aquatic biota. Animals demonstrate, in general, greater tolerance to Fe which may be related to the physiological demand of this metal by the body. Even so, all concentrations of both metals that caused some change in the species represent Brazilian environmental occurrences or Brazilian legislation. It highlights the need for updating the guidelines and constant monitoring of aquatic environments, since even in the face of a hypothetical decontamination of the environment, some changes could persist and affect different trophic levels.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686434","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

Co-Administration of a Plantain-Based Diet and Quercetin Modulates Atrazine-Induced Testicular Dysfunction in Rats via Testicular Steroidogenesis and Redox-Inflammatory Processes. 通过睾丸类固醇生成和氧化还原-炎症过程同时服用车前草和槲皮素可调节阿特拉津诱导的大鼠睾丸功能障碍

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-20 DOI: 10.1002/tox.24431

Damilare Emmanuel Rotimi, Olusola Olalekan Elekofehinti, Olarewaju Michael Oluba, Oluyomi Stephen Adeyemi

{"title":"Co-Administration of a Plantain-Based Diet and Quercetin Modulates Atrazine-Induced Testicular Dysfunction in Rats via Testicular Steroidogenesis and Redox-Inflammatory Processes.","authors":"Damilare Emmanuel Rotimi, Olusola Olalekan Elekofehinti, Olarewaju Michael Oluba, Oluyomi Stephen Adeyemi","doi":"10.1002/tox.24431","DOIUrl":"https://doi.org/10.1002/tox.24431","url":null,"abstract":"Plantain has been reported to enhance testicular function indices, however, the mechanism remains unknown. The present study investigated the action mechanisms of a plantain-based diet in the treatment of rat testicular dysfunction caused by exposure to atrazine (ATZ). The rats were grouped into 10 groups (5 rats each); control group, 50% plantain-based diet (50% PBD), 25% PBD, 12.5% PBD, quercetin (QUE), ATZ only, 50% PBD + ATZ, 25% PBD + ATZ, 12.5% PBD + ATZ, and QUE + ATZ for 21 days. Results revealed that ATZ treatments in rats lowered gonadal hormone levels and the semen quality (sperm concentration, motility, count, and viability), damaged testicular morphology and functions, and impaired redox-inflammatory balance as well as cholinergic and purinergic activities. However, treatment with PBD and QUE ameliorated the testicular toxicity induced by ATZ, although the treatment did not improve the rat semen quality. In addition, the ATZ + QUE and QUE groups showed mild to moderate atrophic degenerative changes, with reduced spermatogenic activity. Together, the results are evidence that 21 days of exposure to ATZ impaired testicular function. However, co-administration of atrazine and PBD improves rat gonadal hormones, redox state, inflammatory indices, cholinergic, and purinergic activities, as well as histoarchitecture of the testes.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675244","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

The Chinese Herbal Medicine Li Qi Huo Xue Di Wan Ameliorates Ischemia or Hypoxia‐Induced Cardiac Injury and Remodeling in the Heart Through a Mechanism Involving Reduction of Necroptosis 中药六味地黄丸通过减少坏死机制改善缺血缺氧诱导的心脏损伤和重塑

IF 4.5 3区医学

Environmental Toxicology Pub Date : 2024-11-12 DOI: 10.1002/tox.24435

Yi‐Yue Zhang, Can Tang, Ya‐Qi Dou, Xiu‐Ju Luo, Jian Pu, Jun Peng

{"title":"The Chinese Herbal Medicine Li Qi Huo Xue Di Wan Ameliorates Ischemia or Hypoxia‐Induced Cardiac Injury and Remodeling in the Heart Through a Mechanism Involving Reduction of Necroptosis","authors":"Yi‐Yue Zhang, Can Tang, Ya‐Qi Dou, Xiu‐Ju Luo, Jian Pu, Jun Peng","doi":"10.1002/tox.24435","DOIUrl":"https://doi.org/10.1002/tox.24435","url":null,"abstract":"Li Qi Huo Xue Di Wan (LQHXDW), a Chinese herbal medicine, is commonly used to treat symptoms such as palpitations, chest tightness, chest pain, and shortness of breath. However, its potential to reduce ischemia or hypoxia‐induced cardiac injury and remodeling, along with the precise mechanisms involved, remains unclear. This study aims to investigate the effects of LQHXDW on cardiac injury and remodeling induced by ischemia or hypoxia, both in vivo and in vitro, and to elucidate the underlying mechanisms. The mouse heart was subjected to ischemia for 14 days, showing evident myocardial injury and notable cardiac remodeling, accompanied by a reduction in cardiac function; these phenomena were reversed in the presence of LQHXDW. In the cultured cardiomyocyte exposed to hypoxia, incubation with LQHXDW increased the cell viability and reduced lactate dehydrogenase release. Mechanistically, LQHXDW exerted inhibitory effect on the phosphorylation levels of RIPK1, RIPK3, and MLKL as well as oxidative stress in the mice hearts suffered ischemia and the cultured cardiomyocytes exposed to hypoxia. Using the methods of ultra‐high performance liquid chromatography‐quadrupole time‐of‐flight‐mass spectrometry, network pharmacology, and cellular thermal shift assay, phenethyl caffeate and isoliquiritigenin were identified as the potential active compounds in LQHXDW that counteract necroptosis. Based on these observations, we conclude that LQHXDW protects the heart against ischemia or hypoxia‐induced cardiac injury and remodeling through suppression of the RIPK1/RIPK3/MLKL pathway‐dependent necroptosis and oxidative stress.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":"19 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142601237","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

MCM4 Promotes the Progression of Malignant Melanoma by Activating the PI3K/AKT Pathway. MCM4 通过激活 PI3K/AKT 通路促进恶性黑色素瘤的进展

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-11-06 DOI: 10.1002/tox.24433

Xuewei Zhang, Mingming Dong, Guoxing Zheng, Meng Sun, Chuzhao Zhang, Zibin Zhou, Shijie Tang

{"title":"MCM4 Promotes the Progression of Malignant Melanoma by Activating the PI3K/AKT Pathway.","authors":"Xuewei Zhang, Mingming Dong, Guoxing Zheng, Meng Sun, Chuzhao Zhang, Zibin Zhou, Shijie Tang","doi":"10.1002/tox.24433","DOIUrl":"https://doi.org/10.1002/tox.24433","url":null,"abstract":"This study aims to elucidate the role of minichromosome maintenance protein 4 (MCM4) in malignant melanoma (MM) and explore the underlying mechanism. Initially, data from The Cancer Genome Atlas (TCGA) database and the Molecular Signature Database (MSigDB) were used to investigate the biological impact of MCM4 on MM. Further, a prognostic model using Cox regression analysis was developed to predict the overall survival (OS) rate in the MM patients. The effects of MCM4 on the proliferation, migration, and invasion abilities of MM (B16F0 and A375) cells were demonstrated using the CCK-8, colony formation, EDU, wound scratch, and Transwell assays. In subcutaneous tumor models in C57BL/6 mice in vivo, the expression levels of MCM4 in MM cells and tumors were detected using Western blot and immunofluorescence approaches. The bioinformatics analysis indicated that MCM4 was expressed higher in MM tissues than in the normal tissues (p < 0.05). The established OS prediction model could significantly contribute to devising follow-up strategies and treating MM patients. MCM4 knockdown resulted in reduced proliferation, migration, and invasion abilities of MM cells, which were reversed by MCM4 overexpression (p < 0.05). Moreover, MCM4 could activate the phosphatidylinositol 3'-kinase (PI3K)/AKT pathway in MM cells. The PI3K inhibitor (LY294002) could reverse the effects of MCM4 on MM cells. MCM4 could substantially prompt the tumor growth of MM in mice through the PI3K/AKT pathway in vivo. In summary, MCM4 prompted the development and metastasis of MM by activating the PI3K/AKT pathway.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582557","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

SERPING1 Reduces Cell Migration via ERK-MMP2-MMP-9 Cascade in Sorafenib- Resistant Hepatocellular Carcinoma. SERPING1 通过 ERK-MMP2-MMP-9 级联降低索拉非尼耐药肝细胞癌的细胞迁移率

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-10-30 DOI: 10.1002/tox.24434

Ching-Chuan Hsieh, Yuh-Harn Wu, Yi-Li Chen, Chun-I Wang, Chao-Jen Li, I-Hsiu Liu, Chen-Wei Chou, Yang-Hsiang Lin, Po-Shuan Huang, Te-Chia Huang, Cheng-Yi Chen

{"title":"SERPING1 Reduces Cell Migration via ERK-MMP2-MMP-9 Cascade in Sorafenib- Resistant Hepatocellular Carcinoma.","authors":"Ching-Chuan Hsieh, Yuh-Harn Wu, Yi-Li Chen, Chun-I Wang, Chao-Jen Li, I-Hsiu Liu, Chen-Wei Chou, Yang-Hsiang Lin, Po-Shuan Huang, Te-Chia Huang, Cheng-Yi Chen","doi":"10.1002/tox.24434","DOIUrl":"https://doi.org/10.1002/tox.24434","url":null,"abstract":"Hepatocellular carcinoma (HCC) is the most common primary hepatic malignant tumor, and it ranks 2nd in terms of mortality rate among all malignancies in Taiwan. Sorafenib is a multiple tyrosine kinase inhibitor that suppresses tumor cell proliferation and angiogenesis around tumors via different pathways. However, the survival outcome of advanced HCC patients treated with sorafenib is still unsatisfactory. Unfortunately, there are no clinically applicable biomarkers to predict sorafenib therapeutic efficiency in HCC thus far. We found that serpin peptidase inhibitor, clade G, member 1 (SERPING1) is highly associated with overall and recurrence-free survival rates in HCC patients and is also highly correlated with several clinical parameters. SERPING1 expression was increased with sorafenib in both the HCC cell extract and conditioned medium, which was also observed in sorafenib-resistant HepG2 and Huh7 cells. Sorafenib decreased cell viability and migration, which was similar to the effect of SERPING1 in HCC progression. Moreover, sorafenib inhibited both MMP-2 and MMP-9 activity and enhanced the expression of p-ERK in HCC cells. In summary, sorafenib reduces HCC cancer progression might through the p-ERK-MMP-2-MMP-9 cascade via upregulation of SERPING1. In the present study, the roles and molecular mechanisms of SERPING1 and its value as a marker for predicting sorafenib resistance and progression in HCC patients were examined. The results of the present study provide a deep understanding of the roles of SERPING1 in HCC sorafenib resistance, which can be applied to develop early diagnosis and prognosis evaluation methods and establish novel therapeutic targets for specifically treating HCC.","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544454","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

Correction to "Inflammatory Response and Endothelial Dysfunction in the Hearts of Mice Co-Exposed to SO2, NO2, and PM2.5". 更正 "共同暴露于二氧化硫、二氧化氮和 PM2.5 的小鼠心脏的炎症反应和内皮功能障碍"。

IF 4.4 3区医学

Environmental Toxicology Pub Date : 2024-10-29 DOI: 10.1002/tox.24432

引用次数: 0