Frontiers in bioscience (Landmark edition)最新文献

{"title":"RETRACTED: Sun <i>et al</i>. Astragaloside IV inhibits human colorectal cancer cell growth. Front. Biosci. (Landmark Ed) 2019, 24(3), 597-606.","authors":"Frontiers In Bioscience-Landmark Editorial Office","doi":"10.31083/j.fbl2912423","DOIUrl":"10.31083/j.fbl2912423","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"423"},"PeriodicalIF":3.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VPO1 Promotes Programmed Necrosis of Cardiomyocytes in Rats with Chronic Heart Failure by Upregulating CYLD.","authors":"Yinzhuang Zhang, Zhijie Shen, Zhuoni Mao, Dan Huang, Chengyu Lou, Li Fang","doi":"10.31083/j.fbl2912425","DOIUrl":"https://doi.org/10.31083/j.fbl2912425","url":null,"abstract":"<p><strong>Background: </strong>Chronic heart failure (CHF) is a serious cardiovascular condition. Vascular peroxidase 1 (VPO1) is associated with various cardiovascular diseases, yet its role in CHF remains unclear. This research aims to explore the involvement of VPO1 in CHF.</p><p><strong>Methods: </strong>CHF was induced in rats using adriamycin, and the expression levels of VPO1 and cylindromatosis (CYLD) were assessed. In parallel, the effects of VPO1 on programmed necrosis in H9c2 cells were evaluated through cell viability assays, lactate dehydrogenase (LDH) level measurements, and analysis of receptor-interacting protein kinase 1/receptor-interacting protein kinase 3/mixed lineage kinase domain-like protein (RIPK1/RIPK3/MLKL) pathway-related proteins. The impact of CYLD on RIPK1 protein stability and ubiquitination was also investigated, along with the interaction between VPO1 and CYLD. Additionally, cardiac structure and function were assessed using echocardiography, Hematoxylin-eosin (HE) staining, Masson staining, and measurements of myocardial injury-related factors, including N-terminal prohormone of brain natriuretic peptide (NT-proBNP), Aspartate aminotransferase (AST), LDH, and creatine kinase-myocardial band (CK-MB).</p><p><strong>Results: </strong>VPO1 expression was upregulated in CHF rats and in H9c2 cells treated with adriamycin. In cellular experiments, VPO1 knockdown improved cell viability, inhibited necrosis and the expression of proteins associated with the RIPK1/RIPK3/MLKL pathway. Mechanistically, VPO1 promoted cardiomyocyte programmed necrosis by interacting with the deubiquitinating enzyme CYLD, which enhanced RIPK1 ubiquitination and degradation, leading to activation of the RIPK1/RIPK3/MLKL signaling pathway. At animal level, overexpression of CYLD counteracted the cardiac failure, cardiac hypertrophy, myocardial injury, myocardial fibrosis, and tissue necrosis caused by VPO1 knockdown.</p><p><strong>Conclusions: </strong>VPO1 exacerbates cardiomyocyte programmed necrosis in CHF rats by upregulating CYLD, which activates the RIPK1/RIPK3/MLKL signaling pathway. Thus, VPO1 may represent a potential therapeutic target for CHF.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"425"},"PeriodicalIF":3.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Display between HPV Infection and Host Immunity in Cervical Cancer.","authors":"Yuanyuan Gu, Tingting Li, Menglei Zhang, Junhao Chen, Fang Shen, Jingxin Ding, Guannan Zhou, Keqin Hua","doi":"10.31083/j.fbl2912426","DOIUrl":"10.31083/j.fbl2912426","url":null,"abstract":"<p><p>Most cervical cancers are related to the persistent infections of high-risk Human Papillomavirus (HPV) infections. Increasing evidence has witnessed the immunosuppressive effectiveness of HPV in the oncogenesis steps and progression steps. Here we review the immune response in HPV-related cervical malignancies and discuss the crosstalk between HPVs and the host immune response. Furthermore, we describe the identification and development of current immunotherapies in cervical cancer. Above all, we hope to provide a novel insight of the display between HPV infections and the host immune system.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"426"},"PeriodicalIF":3.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Hypoxia Induced by Medicinal Plants; A Revolutionary Era of Cellular and Molecular Herbal Medicine in Neuroblastoma Treatment.","authors":"Samin Rahimi, Fatemeh Shirin, Mahdi Moassesfar, Hossein Zafari, Nazila Bahmaie, Kimia Baghebani, Yasna Bidmeshki, Seyede Masoumeh Sajjadi Manesh, Kasra Rasoulzadeh Darabad, Massoud Bahmaie, Elham Nouri, Ahmet Kilic, Melika Ansarin, Pınar Özışık, Ender Simsek, Ozen Ozensoy Guler","doi":"10.31083/j.fbl2912422","DOIUrl":"10.31083/j.fbl2912422","url":null,"abstract":"<p><p>As one of the most common solid pediatric cancers, Neuroblastoma (NBL) accounts for 15% of all of the cancer-related mortalities in infants with increasing incidence all around the world. Despite current therapeutic approaches for NBL (radiotherapies, surgeries, and chemotherapies), these approaches could not be beneficial for all of patients with NBL due to their low effectiveness, and some severe side effects. These challenges lead basic medical scientists and clinical specialists toward an optimal medical interventions for clinical management of NBL. Regardingly, taking molecular and cellular immunopathophysiology involved in the hypoxic microenvironment of NBL into account, it can practically be a contributing approach in the development of \"molecular medicine\" for treatment of NBL. Interestingly, pivotal roles of \"herbal medicine\" in the hypoxic microenvironment of NBL have been extensively interrogated for treating a NBL, functionally being served as an anti-cancer agent via inducing a wide range of molecular and cellular signaling, like apoptosis, cell cycle arrest, and inhibiting angiogenesis. Hence, in this review study, the authors aim to summarize the anti-tumor effects of some medicinal plants and their phytoconstituents through molecular immunopathophysiological mechanisms involved in the hypoxic microenvironment of NBL. In addition, they try to open promising windows to immune gene-based therapies for NBL \"precision medicine\" through clinical advantages of herbal and molecular medicine. An interdisciplinary collaboration among translation and molecular medicine specialists, immunobiologists, herbal medicine specialists, and pediatric neuro-oncologists is highly recommended.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"422"},"PeriodicalIF":3.3,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined Use of Intranasal Methylprednisolone and Allopregnanolone: Revisiting Anti-inflammatory and Remyelinating Treatment in a Murine Model of Multiple Sclerosis.","authors":"Iván Nicolás Pérez-Osorio, José Alejandro Espinosa-Cerón, Camila Álvarez-Gutiérrez, Rodrigo Gonzalez-Flores, Hugo Besedovsky, Gladis Fragoso, Mónica A Torres-Ramos, Edda Sciutto","doi":"10.31083/j.fbl2912420","DOIUrl":"https://doi.org/10.31083/j.fbl2912420","url":null,"abstract":"<p><strong>Background: </strong>Multiple sclerosis (MS) is a demyelinating, neuroinflammatory, progressive disease that severely affects human health of young adults. Neuroinflammation (NI) and demyelination, as well as their interactions, are key therapeutic targets to halt or slow disease progression. Potent steroidal anti-inflammatory drugs such as methylprednisolone (MP) and remyelinating neurosteroids such as allopregnanolone (ALLO) could be co-administered intranasally to enhance their efficacy by providing direct access to the central nervous system (CNS).</p><p><strong>Methods: </strong>The individual and combined effects of MP and ALLO to control the clinical score of murine experimental autoimmune encephalitis (EAE), to preserve spinal cord tissue integrity, modulate cellular infiltration and gliosis, promote remyelination, and modify the expression of Aryl hydrocarbon receptor (AhR) were evaluated. <i>In silico</i> studies, to deep insight into the mechanisms involved for the treatments, were also conducted.</p><p><strong>Results: </strong>MP was the only treatment that significantly reduced the EAE severity, infiltration of inflammatory cells and ionized calcium-binding adapter molecule 1 (<i>Iba-1</i>) expression respect to those EAE non-treated mice but with no-significant differences between the three treatments. MP, ALLO and MP+ALLO significantly reduced tissue damage, AhR expression, and promoted remyelination. Overall, these results suggest that MP, with or without the co-administration with ALLO is an effective and safe strategy to reduce the inflammatory status and the progression of EAE. Despite the expectations of the use of ALLO to reduce the inflammation in EAE, its effect in the dose-scheme used herein is limited only to improve myelination, an effect that supports its usefulness in demyelinating diseases. These results indicate the interest in exploring different doses of ALLO to recommend its use.</p><p><strong>Conclusions: </strong>ALLO treatment mainly maintain the integrity of the spinal cord tissue and the presence of myelin without affecting NI and the clinical outcome. AhR could be involved in the effect observed in both, MP and ALLO treatments. These results will help in the development of a more efficient therapy for MS patients.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"420"},"PeriodicalIF":3.3,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulated METTL3 Accumulates TERT Expression that Promote the Progression of Ovarian Endometriosis.","authors":"Fang Li, Hua Tao, Yini Wei, Ru Meng, Yushan Li, Lifang Nie, Yu Zhang, Jinjun Chang","doi":"10.31083/j.fbl2912421","DOIUrl":"https://doi.org/10.31083/j.fbl2912421","url":null,"abstract":"<p><strong>Background: </strong>Endometriosis is a complicated and enigmatic disease that significantly diminishes the quality of life for women affected by this condition. Increased levels of human telomerase reverse transcriptase (<i>TERT</i>) mRNA and telomerase activity have been found in the endometrium of these patients. However, the precise function of TERT in endometriosis and the associated biological mechanisms remain poorly understood.</p><p><strong>Methods: </strong>We analyzed TERT expression in ectopic endometrial (EC), eutopic endometrial (EU), and normal endometrial (NC) tissues. Human endometrial stromal cells (HESCs) were used to study the effects of TERT depletion and knockdown on cell behavior. We also assessed methyltransferase-like 3 (METTL3)-mediated N6-methyladenosine (m6A) modification in <i>TERT</i> transcripts and its impact on mRNA stability and cell functions.</p><p><strong>Results: </strong>The current results indicate that TERT expression is elevated in EC tissue compared to both EU and NC. Depletion of <i>TERT</i> suppressed the proliferation and migration of HESCs, while <i>TERT</i> overexpression had the opposite effect. We found high levels of METTL3-mediated m6A modification in <i>TERT</i> transcripts, particularly in the coding sequence region, resulting in increased translation. However, EC tissues had lower m6A levels due to the downregulation of METTL3. Mechanistically, m6A modification mediated by METTL3 negatively regulates the stability of <i>TERT</i> mRNA in a YTH N6-methyladenosine RNA binding protein 2 (YTHDF2)-dependent manner. Furthermore, METTL3 negatively regulated the proliferation and migration of HESCs.</p><p><strong>Conclusions: </strong>Together, our study identified a new molecular mechanism that underlies the pathogenesis of endometriosis. Inhibition of m6A modification and of the METTL3/TERT axis may enhance cellular proliferation and migration, thereby contributing to the progression of endometriosis.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"421"},"PeriodicalIF":3.3,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanism and Clinical Significance of Sperm DNA Damage in Assisted Reproductive.","authors":"Kangsheng Liu, Yajun Chen, Ruifang An","doi":"10.31083/j.fbl2912416","DOIUrl":"https://doi.org/10.31083/j.fbl2912416","url":null,"abstract":"<p><p>The prevalence of sperm DNA fragmentation (SDF) is significantly higher in males with infertility, which is often associated with oligozoospermia and hypospermia. It can also occur in patients with infertility who have normal conventional semen indicators. The etiologies involve aberrations in sperm maturation, dysregulated apoptotic processes, and heightened levels of oxidative stress. In this article, we retrieved PubMed, China National Knowledge Infrastructure (CNKI) and Web of Science databases for articles and reviews published before February 28, 2024. Using \"sperm DNA fragments; assisted reproductive technology, mechanism, clinical pregnancy outcome\" as keywords, and comprehensively reviewed on their basis. Numerous literature sources have reported an increased utilization of SDF testing in the context of male infertility, as there is a negative correlation between SDF levels and the success of natural conception as well as assisted reproductive technologies. To enhance the clinical outcome for individuals experiencing infertility, investigating the prevalence and underlying mechanisms of sperm DNA damage is beneficial. This review article delves into the mechanisms that lead to sperm DNA damage and assesses the impact of DNA fragmentation index (DFI) on pregnancy outcomes in the context of assisted reproductive technologies.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"416"},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Innate Priming in Modifying Tumor-associated Macrophage Phenotype.","authors":"Ben Topham, Barry Hock, Elisabeth Phillips, George Wiggins, Margaret Currie","doi":"10.31083/j.fbl2912418","DOIUrl":"10.31083/j.fbl2912418","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) are innate immune cells that exert far reaching influence over the tumor microenvironment (TME). Depending on cues within the local environment, TAMs may promote tumor angiogenesis, cancer cell invasion and immunosuppression, or, alternatively, inhibit tumor progression via neoantigen presentation, tumoricidal reactive oxygen species generation and pro-inflammatory cytokine secretion. Therefore, TAMs have a pivotal role in determining tumor progression and response to therapy. TAM phenotypes are driven by cytokines and physical cues produced by tumor cells, adipocytes, fibroblasts, pericytes, immune cells, and other cells within the TME. Research has shown that TAMs can be primed by environmental stimuli, adding another layer of complexity to the environmental context that determines TAM phenotype. Innate priming is a functional consequence of metabolic and epigenetic reprogramming of innate cells by a primary stimulant, resulting in altered cellular response to future secondary stimulation. Innate priming offers a novel target for development of cancer immunotherapy and improved prognosis of disease, but also raises the risk of exacerbating existing inflammatory pathologies. This review will discuss the mechanisms underlying innate priming including metabolic and epigenetic modification, its relevance to TAMs and tumor progression, and possible clinical implications for cancer treatment.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"418"},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The PKM2/HIF-1α Axis is Involved in the Pathogenesis of Endometriosis via TGF-β1 under Endometrial Polyps.","authors":"Jianjuan Li, Li Liu, Ruiqi Fan","doi":"10.31083/j.fbl2912417","DOIUrl":"https://doi.org/10.31083/j.fbl2912417","url":null,"abstract":"<p><strong>Background: </strong>Endometriosis patients exhibit a cancer-like glycolytic phenotype. The pyruvate kinase M2 (PKM2)/hypoxia-inducible factor-1 alpha (HIF-1α) axis plays important roles in glycolysis-related diseases, but its role in patients with endometrial polyps (EPs) combined with endometriosis has not been validated.</p><p><strong>Methods: </strong>EP samples were collected from patients with and without endometriosis. PKM2, HIF-1α, and transforming growth factor-beta 1 (TGF-β1) levels were detected by immunohistochemistry (IHC), quantitative polymerase chain reaction, western blotting, and/or immunofluorescence. Primary endometrial stromal cells (ESCs) and non-endometriotic patient-derived ESCs (NESCs) were isolated from patients with EP with or without endometriosis. PKM2 loss-of-function assays in ESCs and gain-of-function assays in NESCs were performed to assess the function of PKM2. The effects of PKM2 and TGF-β1 on the promoter activity of HIF-1α were determined by dual-luciferase reporter assay.</p><p><strong>Results: </strong>PKM2 was overexpressed in ESCs compared to NESCs. Furthermore, PKM2 knockdown repressed viability, decreased migration and invasion, and restrained glycolysis of ESCs, accompanied by reduced HIF-1α levels and weakened promoter activity of HIF-1α. In addition, PKM2 overexpression had the opposite effect on these indicators in NESCs. Of note, an anti-TGF-β1 Ab reversed the PKM2-overexpression-mediated effects on cell viability, migration, and invasion, but not glycolysis or HIF-1α promoter activity, in NESCs. Additionally, PKM2, HIF-1α, and TGF-β1 levels were higher in EP samples with endometriosis than in EP samples without endometriosis, and there were positive correlations between PKM2, HIF-1α, and TGF-β1 IHC scores in all EP samples.</p><p><strong>Conclusions: </strong>PKM2/HIF-1α-axis-dependent glycolysis participates in the pathogenesis of EP combined with endometriosis by mediating TGF-β1 signaling.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"417"},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Zeng et al. Silencing NEAT1 suppresses thyroid carcinoma via miR-126/NEAT1/VEGFA axis. Frontiers in Bioscience (Landmark Edition). 2020; 25: 564-576.","authors":"Frontiers In Bioscience-Landmark Editorial Office","doi":"10.31083/j.fbl2912419","DOIUrl":"10.31083/j.fbl2912419","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"419"},"PeriodicalIF":3.3,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}