Anti-Cancer Drugs最新文献_第7页

Dermatological toxicity associated with the use of gilteritinib in relapsed acute myeloid leukemia with FLT3 mutation: a case report. 在FLT3基因突变的复发急性髓性白血病患者中使用吉特替尼引起的皮肤毒性：病例报告。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-08 DOI: 10.1097/CAD.0000000000001634

Alicia Martín Roldán, Carolina Alarcón-Payer, María Del Mar Sánchez Suárez, Alberto Jiménez Morales

引用次数: 0

Rituximab-induced leukocytoclastic vasculitis in a patient with low-grade orbital B-cell lymphoma: a case report. 一名低级别眼眶 B 细胞淋巴瘤患者的利妥昔单抗诱发白细胞破坏性血管炎：病例报告。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-23 DOI: 10.1097/CAD.0000000000001638

Nesime İnci Güner, Ömer Dizdar, Alev Türker, Aygin Bayraktar-Ekincioglu

引用次数: 0

Targeting xCT with sulfasalazine suppresses triple-negative breast cancer growth via inducing autophagy and coordinating cell cycle and proliferation. 通过诱导自噬和协调细胞周期与增殖，磺胺嘧啶靶向 xCT 可抑制三阴性乳腺癌的生长。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-01 DOI: 10.1097/CAD.0000000000001630

Yaping Long, Zizheng Xu, Jing Yu, Xiao Hu, Yu Xie, Xianxian Duan, Ning Li, Yan Yan, Yue Wang, Junfang Qin

{"title":"Targeting xCT with sulfasalazine suppresses triple-negative breast cancer growth via inducing autophagy and coordinating cell cycle and proliferation.","authors":"Yaping Long, Zizheng Xu, Jing Yu, Xiao Hu, Yu Xie, Xianxian Duan, Ning Li, Yan Yan, Yue Wang, Junfang Qin","doi":"10.1097/CAD.0000000000001630","DOIUrl":"10.1097/CAD.0000000000001630","url":null,"abstract":"There is a substantial unmet need for effective treatment strategies in triple-negative breast cancer (TNBC). Recently, renewed attention has been directed towards targeting glutamine (Gln) metabolism to enhance the efficacy of cancer treatment. Nonetheless, a comprehensive exploration into the mechanistic implications of targeting Gln metabolism in TNBC is lacking. In this study, our objective was to probe the sensitivity of TNBC to alterations in Gln metabolism, using representative TNBC cell lines: MDA-MB-231, MDA-MB-468, and 4T1. Through an integration of bioinformatics, in-vitro, and in-vivo investigations, we demonstrated that sulfasalazine (SAS), like erastin (a known xCT inhibitor), effectively suppressed the expression and transport function of xCT, resulting in a depletion of glutathione levels in MDA-MB-231 and MDA-MB-468 cells. Furthermore, both xCT knockdown and SAS treatment demonstrated the promotion of cellular autophagy. We unveiled a positive correlation between xCT and the autophagy-related molecule p62, their co-expression indicating poor survival outcomes in breast cancer patients. In addition, our research revealed the influence of SAS and xCT on the expression of proteins regulating cell cycle and proliferation. Treatment with SAS or xCT knockdown led to the inhibition of MYC, CDK1, and CD44 expression. Significantly, the combined administration of SAS and rapamycin exhibited a synergistic inhibitory effect on the growth of transplanted breast tumor in mouse models constructed from murine-derived 4T1 cells. Taken together, our findings suggested the potential and clinical relevance of the SAS and rapamycin combination in the treatment of TNBC.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"830-843"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141625796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Regulation of cervical cancer via G15-mediated inhibition of G protein-coupled estrogen receptor. 通过 G15 介导的 G 蛋白偶联雌激素受体抑制宫颈癌的发生。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-17 DOI: 10.1097/CAD.0000000000001640

Ziyan Zhu, Xinyi Nie, Lexiu Deng, Jia Ding, Jiangping Chen, Jingyi Zhu, Xiaoxia Yin, Bowei Guo, Fan Zhang

{"title":"Regulation of cervical cancer via G15-mediated inhibition of G protein-coupled estrogen receptor.","authors":"Ziyan Zhu, Xinyi Nie, Lexiu Deng, Jia Ding, Jiangping Chen, Jingyi Zhu, Xiaoxia Yin, Bowei Guo, Fan Zhang","doi":"10.1097/CAD.0000000000001640","DOIUrl":"10.1097/CAD.0000000000001640","url":null,"abstract":"Cervical cancer is among the most common gynecological malignancies. G protein-coupled estrogen receptor (GPER) is involved in the development of various tumors; however, its role in cervical cancer remains unclear. We investigated whether G15, an inhibitor of GPER, can regulate its expression and affect cervical cancer progression. We examined the biological behaviors of G15-treated SiHa and HeLa cells using Cell Counting Kit-8, monoclonal proliferation, plate scratching, and Transwell invasion experiments. Western blotting was used to detect the expression of GPER, E-cadherin, N-cadherin, vimentin, Bcl-2, Bax, phosphatidylinositol-3-kinase (PI3K)/AKT, and programmed death ligand 1 (PD-L1). The expression of GPER, E-cadherin, vimentin, and PD-L1 in cervical cancer and adjacent tissues was detected using immunohistochemistry. The correlation between GPER expression and clinicopathological characteristics was analyzed. The expression of GPER in cervical cancer tissues was significantly higher than that in paracancerous tissues, and it was detected in the membrane and cytoplasm of SiHa and HeLa cells. The proliferation, migration, and invasion abilities of SiHa and HeLa cells were reduced after G15 treatment. The G15-treated groups exhibited higher expression of E-cadherin and Bax and lower expression of N-cadherin, vimentin, Bcl-2, GPER, p-PI3K, p-AKT, and PD-L1 than the control group. The expression of E-cadherin was lower and that of vimentin was higher in cancer tissues than in paracancerous tissues; PD-L1 was highly expressed in tumor and stromal cells in cancer tissues but not in paracancerous tissues. G15 functions by regulating the GPER/PI3K/AKT/PD-L1 signaling pathway and may serve as a new immunotherapy for treating patients with cervical cancer.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"817-829"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Individualized medication of venetoclax based on therapeutic drug monitoring in Chinese acute myeloid leukemia patients using an HPLC method. 利用高效液相色谱法，基于治疗药物监测对中国急性髓性白血病患者进行韦尼替克的个体化用药。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-08 DOI: 10.1097/CAD.0000000000001632

Yue Tang, Peng Rao, Shuojiao Li, Wenxian Yu, Ranran Wang, Jiatao Liu

{"title":"Individualized medication of venetoclax based on therapeutic drug monitoring in Chinese acute myeloid leukemia patients using an HPLC method.","authors":"Yue Tang, Peng Rao, Shuojiao Li, Wenxian Yu, Ranran Wang, Jiatao Liu","doi":"10.1097/CAD.0000000000001632","DOIUrl":"10.1097/CAD.0000000000001632","url":null,"abstract":"Objective: The aim of this study was to establish a simple and sensitive high-performance liquid chromatography method for therapeutic drug monitoring of venetoclax (VEN) and optimize regimens.Methods: The analysis required the extraction of a 50 μl plasma sample and the precipitation of proteins using acetonitrile extraction. The chromatographic method employed a mobile phase of acetonitrile: 0.5% KH 2 PO 4 (pH 3.5) (60/40, v/v) on a Diamond C 18 (4.6 mm × 250 mm, 5 μm) column at a flow rate of 1.0 ml/min. The quantitative method was validated based on standards described in 'Bioanalytical Method Validation: Guidance for Industry' published by the US Food and Drug Administration (FDA).Results: The calibration curve was linear ( R2 = 0.9998) over the range of 75-4800 ng/ml, with limits of quantification of 25 ng/ml. The coefficients of intraday and interday validation, specificity, recovery, and stability all met the criteria of FDA guidance. The method was successfully applied to analyze VEN concentrations in 30 cases of acute myeloid leukemia patients. The peak concentration ( Cmax ) was 1881.19 ± 756.61 ng/ml, while the trough concentration ( Cmin ) was 1212.69 ± 767.92 ng/ml in acute myeloid leukemia patients.Conclusion: Our study establishes a simple, precise, and sensitive high-performance liquid chromatography method for monitoring VEN and confirms its applicability for therapeutic drug monitoring of VEN in hematological cancers.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"852-858"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Donafenib inhibits PARP1 expression and induces DNA damage, in combination with PARP1 inhibitors promotes apoptosis in liver cancer cells. 多奈非尼可抑制 PARP1 的表达并诱导 DNA 损伤，与 PARP1 抑制剂联合使用可促进肝癌细胞凋亡。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-06-26 DOI: 10.1097/CAD.0000000000001631

Jiuliang Jiang, Pingping Yang, Xinyu Xu, Huixiong Yuan, Haitao Zhu

{"title":"Donafenib inhibits PARP1 expression and induces DNA damage, in combination with PARP1 inhibitors promotes apoptosis in liver cancer cells.","authors":"Jiuliang Jiang, Pingping Yang, Xinyu Xu, Huixiong Yuan, Haitao Zhu","doi":"10.1097/CAD.0000000000001631","DOIUrl":"10.1097/CAD.0000000000001631","url":null,"abstract":"Liver cancer is a prevalent malignant tumor globally. The newly approved first-line drug, donafenib, is a novel oral small molecule multi-tyrosine kinase inhibitor that has significant antitumor effects on liver cancer. This study aims to investigate the antitumor effects of donafenib on liver cancer and to explore its potential mechanisms. Donafenib significantly inhibited the viability of Huh-7 and HCCLM3 cells, inhibited malignant cell proliferation, and promoted cell apoptosis, as demonstrated by CCK-8, EdU, and Calcein/PI (propidium iodide) staining experiments. The results of DNA damage detection experiments and western blot analysis indicate that donafenib caused considerable DNA damage in liver cancer cells. The analysis of poly (ADP-ribose) polymerase 1 (PARP1) in liver cancer patients using online bioinformatics data websites such as TIMER2.0, GEPIA, UALCAN, cBioPortal, Kaplan-Meier Plotter, and HPA revealed a high expression of PARP1, which is associated with poor prognosis. Molecular docking and western blot analysis demonstrated that donafenib can directly target and downregulate the protein expression of PARP1, a DNA damage repair protein, thereby promoting DNA damage in liver cancer cells. Western blot and immunofluorescence detection showed that the group treated with donafenib combined with PARP1 inhibitor had significantly higher expression of γ-H2AX and 8-OHdG compared to the groups treated with donafenib or PARP1 inhibitors alone, the combined treatment suppresses the expression of the antiapoptotic protein Bcl2 and enhances the protein expression level of the proapoptotic protein Bcl-2-associated X protein (BAX). These data suggest that the combination of donafenib and a PARP1 inhibitor results in more significant DNA damage in cells and promotes cell apoptosis. Thus, the combination of donafenib and PARP1 inhibitors has the potential to be a treatment option for liver cancer.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"789-805"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Investigation of the synergistic effect mechanism underlying sequential use of palbociclib and cisplatin through integral proteomic and glycoproteomic analysis. 通过完整的蛋白质组和糖蛋白组分析，研究连续使用帕博西尼和顺铂的协同效应机制。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-08 DOI: 10.1097/CAD.0000000000001633

Lulu Yang, Bo Meng, Xiaoyun Gong, You Jiang, Xuping Shentu, Zhichao Xue

{"title":"Investigation of the synergistic effect mechanism underlying sequential use of palbociclib and cisplatin through integral proteomic and glycoproteomic analysis.","authors":"Lulu Yang, Bo Meng, Xiaoyun Gong, You Jiang, Xuping Shentu, Zhichao Xue","doi":"10.1097/CAD.0000000000001633","DOIUrl":"10.1097/CAD.0000000000001633","url":null,"abstract":"Chemoresistance largely hampers the clinical use of chemodrugs for cancer patients, combination or sequential drug treatment regimens have been designed to minimize chemotoxicity and resensitize chemoresistance. In this work, the cytotoxic effect of cisplatin was found to be enhanced by palbociclib pretreatment in HeLa cells. With the integration of liquid chromatography-mass spectrometry-based proteomic and N-glycoproteomic workflow, we found that palbociclib alone mainly enhanced the N-glycosylation alterations in HeLa cells, while cisplatin majorly increased the different expression proteins related to apoptosis pathways. As a result, the sequential use of two drugs induced a higher expression level of apoptosis proteins BAX and BAK. Those altered N-glycoproteins induced by palbociclib were implicated in pathways that were closely associated with cell membrane modification and drug sensitivity. Specifically, the top four frequently glycosylated proteins FOLR1, L1CAM, CD63, and LAMP1 were all associated with drug resistance or drug sensitivity. It is suspected that palbociclib-induced N-glycosylation on the membrane protein allowed the HeLa cell to become more vulnerable to cisplatin treatment. Our study provides new insights into the mechanisms underlying the sequential use of target drugs and chemotherapy drugs, meanwhile suggesting a high-efficiency approach that involves proteomic and N-glycoproteomic to facilitate drug discovery.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"806-816"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11392100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Complete and durable regression of leptomeningeal involvement during lorlatinib treatment in a patient with lung cancer. 一名肺癌患者在接受乐拉替尼治疗期间，其左侧脑膜受累症状完全和持久消退。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-10-01 Epub Date: 2024-07-09 DOI: 10.1097/CAD.0000000000001637

Giorgia Guaitoli, Enrica Martinelli, Lucia Trudu, Isacco Desideri, Pietro Mortini, Stefano Greco, Alessio Bruni, Daniela Greto, Guido Pecchioli, Chiara Chiavelli, Massimo Dominici, Federica Bertolini

{"title":"Complete and durable regression of leptomeningeal involvement during lorlatinib treatment in a patient with lung cancer.","authors":"Giorgia Guaitoli, Enrica Martinelli, Lucia Trudu, Isacco Desideri, Pietro Mortini, Stefano Greco, Alessio Bruni, Daniela Greto, Guido Pecchioli, Chiara Chiavelli, Massimo Dominici, Federica Bertolini","doi":"10.1097/CAD.0000000000001637","DOIUrl":"10.1097/CAD.0000000000001637","url":null,"abstract":"Metastatic spread to the central nervous system (CNS) is frequent in anaplastic lymphoma kinase ( ALK )-rearranged non-small cell lung cancer (NSCLC) and has an important impact on patient prognosis and quality of life. Leptomeningeal involvement may occur in up to 10% of cases of ALK-positive NSCLC. Lorlatinib is a third-generation ALK inhibitor that has excellent CNS penetrability and demonstrated its efficacy both in pretreated and treatment-naive patients. Herein, we present the case of a 34-year-old patient diagnosed with stage IV ALK-rearranged NSCLC who received two lines of ALK inhibitors (crizotinib followed by alectinib) and several courses of brain stereotactic ablative radiotherapy until leptomeningeal involvement was detected. Third-line lorlatinib was then administered, and 2 months later encephalic MRI documented complete regression of the leptomeningeal involvement that is still maintained after 36 months while treatment with lorlatinib is still ongoing with good tolerability. To the best of our knowledge, this is the longer intracranial response reported in the literature, underlining the importance of the most appropriate choice of systemic treatments and their integration with loco-regional approaches to improve outcomes.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"867-871"},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11410147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

MET alterations as resistance mechanisms of dabrafenib-trametinib in BRAF p.V600E mutated non-small cell lung cancer patient. MET改变是BRAF p.V600E突变非小细胞肺癌患者对达拉菲尼-曲美替尼的耐药机制。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-09-01 Epub Date: 2024-05-20 DOI: 10.1097/CAD.0000000000001623

Monica Pluchino, Irene Testi, Roberta Minari, Alessandra Dodi, Giulia Airò, Giulia Mazzaschi, Michela Verzè, Alessia Adorni, Letizia Gnetti, Cinzia Azzoni, Costanza Anna Maria Lagrasta, Federica Pecci, Marcello Tiseo

{"title":"MET alterations as resistance mechanisms of dabrafenib-trametinib in BRAF p.V600E mutated non-small cell lung cancer patient.","authors":"Monica Pluchino, Irene Testi, Roberta Minari, Alessandra Dodi, Giulia Airò, Giulia Mazzaschi, Michela Verzè, Alessia Adorni, Letizia Gnetti, Cinzia Azzoni, Costanza Anna Maria Lagrasta, Federica Pecci, Marcello Tiseo","doi":"10.1097/CAD.0000000000001623","DOIUrl":"10.1097/CAD.0000000000001623","url":null,"abstract":"The combination of BRAF and MEK inhibitors demonstrated significant clinical benefit in patients with BRAF-mutant non-small cell lung cancer (NSCLC). However, the molecular mechanisms of acquired resistance to BRAF and MEK inhibition in NSCLC are still unknown. Herein, we report a case of a 76-year-old man with a history of smoking who was diagnosed with BRAF V600E-mutant lung adenocarcinoma (PD-L1 > 50%) and subsequently candidate to first-line therapy with pembrolizumab. After 18 months since the start of immunotherapy, computed tomography scan showed disease progression and a second-line therapy with dabrafenib and trametinib was initiated. Seven months later, due to a suspect disease progression, a left supraclavicular lymphadenectomy was performed and next-generation sequencing analysis revealed the appearance of MET exon 14 skipping mutation, while fluorescence in situ hybridization analysis showed MET amplification. The patient is still on BRAF and MEK inhibitor treatment. Our case highlights the relevance of performing tumor tissue rebiopsy at the time of progression during treatment with BRAF/MEK inhibition with the aim of identifying putative mechanisms of resistance.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":"35 8","pages":"761-763"},"PeriodicalIF":1.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

TRIM11 expression levels was downregulated and prevents ferroptosis of cardiomyocyte by Dusp6 in acute myocardial infarction. Dusp6 下调了 TRIM11 的表达水平，并阻止了急性心肌梗死中心肌细胞的铁变态反应。

IF 1.8 4区医学

Anti-Cancer Drugs Pub Date : 2024-09-01 Epub Date: 2024-05-03 DOI: 10.1097/CAD.0000000000001614

Xiaofu Wu, Wenyuan Zhang

{"title":"TRIM11 expression levels was downregulated and prevents ferroptosis of cardiomyocyte by Dusp6 in acute myocardial infarction.","authors":"Xiaofu Wu, Wenyuan Zhang","doi":"10.1097/CAD.0000000000001614","DOIUrl":"10.1097/CAD.0000000000001614","url":null,"abstract":"Acute myocardial infarction (AMI) is the high incidence rate and mortality of common cardiovascular disease. Herein, we explored the critical role of TRIM11 in AMI and its underlying mechanism. Serum from patients with AMI were collected from our hospital. Mice of model group received angiotensin II. Mice of model + TRIM11 group received with Ang II and TRIM11 vectors. Mice of sham group received normal saline. H9c2 cells were performed transfections using Lipofectamine 2000 (Thermo Fisher Scientific Inc, Shanghai, China), and treated with Ang II. TRIM11 mRNA expression was reduced, was negative correlation with collagen I/III mRNA expression, systolic blood pressure, diastolic blood pressure, left anteroposterior atrial diameter, right atrial diameter, or left ventricular ejection fraction in patient with AMI. TRIM11 mRNA and protein expression were also suppressed. METTL3 regulates TRIM11 methylation to reduce TRIM11 gene stability in model of AMI. TRIM11 gene ameliorated AMI in mice model. TRIM11 gene reduced reactive oxygen species production level of cardiomyocyte in-vitro model. TRIM11 gene reduced ferroptosis of cardiomyocyte in-vitro model. TRIM11 gene reduced ferroptosis by the inhibition of mitochondrial damage of cardiomyocyte in model of AMI. TRIM11 induced Dusp6 protein expression. Bioluminescence imaging showed that TRIM11 virus increased Dusp6 expression in heart tissue of mice model. The inhibition of Dusp6 reduced the effects of TRIM11 on ferroptosis of cardiomyocyte in model of AMI. In conclusion, this study demonstrates that TRIM11 improves AMI by regulating Dusp6 to inhibit ferroptosis of cardiomyocyte, and suggest a novel target for AMI.","PeriodicalId":7969,"journal":{"name":"Anti-Cancer Drugs","volume":" ","pages":"720-731"},"PeriodicalIF":1.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140890834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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