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Chemokines Signature and T Cell Dynamics in Leishmaniasis: Molecular insight and therapeutic application. 利什曼病中的趋化因子特征和 T 细胞动力学:分子洞察与治疗应用
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-26 DOI: 10.1017/erm.2024.36
Shreya Upadhyay, Shashi Kumar, Vishal Kumar Singh, Rahul Tiwari, Awnish Kumar, Shyam Sundar, Rajiv Kumar
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引用次数: 0
Developing a potent vaccine against Helicobacter pylori: critical considerations and challenges. 开发针对幽门螺旋杆菌的强效疫苗:关键考虑因素和挑战。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-25 DOI: 10.1017/erm.2024.19
Faria Hasanzadeh Haghighi, Shaho Menbari, Roghayeh Mohammadzadeh, Abbas Pishdadian, Hadi Farsiani
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引用次数: 0
Exercise Mediates Noncoding RNAs in Cardiovascular Diseases: Pathophysiological Roles and Clinical Application. 运动介导心血管疾病中的非编码 RNA:病理生理学作用和临床应用。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-21 DOI: 10.1017/erm.2024.25
Changyong Wu, Xiaocui Chen, Lu Yang, Huang Sun, Suli Bao, Haojie Li, Lihui Zheng, Huiling Zeng, Ruijie Li, Yunzhu Peng

Exercise-based cardiac rehabilitation is effective in improving cardiovascular disease risk factor management, cardiopulmonary function, and quality of life. However, the precise mechanisms underlying exercise-induced cardioprotection remain elusive. Recent studies have shed light on the beneficial functions of noncoding RNAs in either exercise or illness models, but only a limited number of noncoding RNAs have been studied in both contexts. Hence, the present study aimed to elucidate the pathophysiological implications and molecular mechanisms underlying the association among exercise, noncoding RNAs, and cardiovascular diseases. Additionally, the present study analysed the most effective and personalized exercise prescription, serving as a valuable reference for guiding the clinical implementation of cardiac rehabilitation in patients with cardiovascular diseases.

以运动为基础的心脏康复在改善心血管疾病危险因素管理、心肺功能和生活质量方面是有效的。然而,运动引起的心脏保护的确切机制仍然难以捉摸。最近的研究已经阐明了非编码rna在运动或疾病模型中的有益功能,但只有有限数量的非编码rna在这两种情况下进行了研究。因此,本研究旨在阐明运动、非编码rna和心血管疾病之间关联的病理生理意义和分子机制。此外,本研究还分析了最有效、最个性化的运动处方,为指导心血管疾病患者心脏康复的临床实施提供有价值的参考。
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引用次数: 0
Exploring the Antifibrotic Mechanisms of Ghrelin: Modulating TGF-β Signalling in Organ Fibrosis. 探索胃泌素的抗纤维化机制:调节器官纤维化中的 TGF-β 信号传导
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-21 DOI: 10.1017/erm.2024.38
Mei Li, Chang Zheng, Huiyi Wang, Shan Wang

Background: Fibrosis is a pathological condition that affects various organs by increasing fibrous connective tissue while reducing parenchymal cells. This imbalance can lead to compromised organ function and potential failure, posing significant health risks. The condition's complexity necessitates the exploration of effective treatments to mitigate its progression and adverse outcomes.

Aims: This study aims to investigate the role of ghrelin, a peptide hormone known for its anti-inflammatory and anti-fibrotic properties, in modulating fibrosis across different organs. By binding to the growth hormone secretagogue receptor type 1a (GHSR-1a), ghrelin has shown potential in attenuating the fibrotic process, particularly through its interaction with the TGF-β signalling pathway.

Methods: An extensive review of clinical and animal model studies focusing on liver, kidney, lung, and myocardial fibrosis was conducted. The primary focus was on examining how ghrelin influences the TGF-β signalling pathway, with an emphasis on the regulation of TGF-β expression and the suppression of Smad signalling molecules. The methodology involved analysing data from various studies to understand ghrelin's molecular mechanisms in combating fibrosis.

Results: The findings from the reviewed studies indicate that ghrelin exerts significant anti-fibrotic effects across multiple organ systems. Specifically, ghrelin was found to downregulate TGF-β expression and suppress Smad signalling molecules, leading to a marked reduction in fibrous tissue accumulation and preservation of organ function. In liver fibrosis models, ghrelin reduced TGF-β1 levels and Smad3 phosphorylation, while in kidney and cardiac fibrosis, similar protective effects were observed. The data also suggest that ghrelin's effects are mediated through both canonical and non-canonical TGF-β pathways.

Conclusions: Ghrelin presents a promising therapeutic agent in the management of fibrosis due to its potent anti-inflammatory and anti-fibrotic actions. Its ability to modulate the TGF-β signalling pathway underscores a vital molecular mechanism through which ghrelin can mitigate fibrotic progression in various organs. Future research should focus on further elucidating ghrelin's molecular interactions and potential clinical applications in fibrosis treatment, offering new avenues for developing effective anti-fibrotic therapies.

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引用次数: 0
Cell therapy in Sjögren's syndrome: opportunities and challenges. 细胞疗法在斯约格伦综合征中的应用:机遇与挑战。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-23 DOI: 10.1017/erm.2024.21
Yangyang Lu, Rongjing Shi, Wenqin He, Qi An, Jingwen Zhao, Xinnan Gao, Baiyan Zhang, Liyun Zhang, Ke Xu, Dan Ma

Sjögren's syndrome (SS) is a chronic autoimmune disease caused by immune system disorders. The main clinical manifestations of SS are dry mouth and eyes caused by the destruction of exocrine glands, such as the salivary and lacrimal glands, and systemic manifestations, such as interstitial pneumonia, interstitial nephritis and vasculitis. The pathogenesis of this condition is complex. However, this has not been fully elucidated. Treatment mainly consists of glucocorticoids, disease-modifying antirheumatic drugs and biological agents, which can only control inflammation but not repair the tissue. Therefore, identifying methods to regulate immune disorders and repair damaged tissues is imperative. Cell therapy involves the transplantation of autologous or allogeneic normal or bioengineered cells into the body of a patient to replace damaged cells or achieve a stronger immunomodulatory capacity to cure diseases, mainly including stem cell therapy and immune cell therapy. Cell therapy can reduce inflammation, relieve symptoms and promote tissue repair and regeneration of exocrine glands such as the salivary glands. It has broad application prospects and may become a new treatment strategy for patients with SS. However, there are various challenges in cell preparation, culture, storage and transportation. This article reviews the research status and prospects of cell therapies for SS.

斯约格伦综合征(SS)是一种由免疫系统紊乱引起的慢性自身免疫性疾病。SS的主要临床表现是唾液腺和泪腺等外分泌腺受到破坏而引起的口干和眼干,以及间质性肺炎、间质性肾炎和血管炎等全身表现。这种疾病的发病机制十分复杂。然而,这一点尚未完全阐明。治疗方法主要包括糖皮质激素、改善病情抗风湿药物和生物制剂,但这些药物只能控制炎症,不能修复组织。因此,找到调节免疫紊乱和修复受损组织的方法势在必行。细胞疗法是指将自体或异体正常细胞或生物工程细胞移植到患者体内,以替代受损细胞或获得更强的免疫调节能力,从而达到治疗疾病的目的,主要包括干细胞疗法和免疫细胞疗法。细胞疗法可以减轻炎症,缓解症状,促进唾液腺等外分泌腺组织的修复和再生。它具有广阔的应用前景,有可能成为 SS 患者的一种新的治疗策略。然而,在细胞制备、培养、储存和运输方面存在各种挑战。本文回顾了细胞疗法治疗 SS 的研究现状和前景。
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引用次数: 0
Radiation drives tertiary lymphoid structures to reshape TME for synergized antitumour immunity. 辐射驱动三级淋巴结构重塑 TME,以实现协同抗肿瘤免疫。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-23 DOI: 10.1017/erm.2024.27
Shuling Li, Kuifei Chen, Zhenwei Sun, Meng Chen, Wenhu Pi, Suna Zhou, Haihua Yang

Radiotherapy (RT) plays a key role in the tumour microenvironment (TME), impacting the immune response via cellular and humoral immunity. RT can induce local immunity to modify the TME. It can stimulate dendritic cell maturation and T-cell infiltration. Moreover, B cells, macrophages and other immune cells may also be affected. Tertiary lymphoid structure (TLS) is a unique structure within the TME and a class of aggregates containing T cells, B cells and other immune cells. The maturation of TLS is determined by the presence of mature dendritic cells, the density of TLS is determined by the number of immune cells. TLS maturation and density both affect the antitumour immune response in the TME. This review summarized the recent research on the impact and the role of RT on TLS, including the changes of TLS components and formation conditions and the mechanism of how RT affects TLS and transforms the TME. RT may promote TLS maturation and density to modify the TME regarding enhanced antitumour immunity.

放疗(RT)在肿瘤微环境(TME)中发挥着关键作用,通过细胞和体液免疫影响免疫反应。RT 可诱导局部免疫以改变肿瘤微环境。它可以刺激树突状细胞成熟和 T 细胞浸润。此外,B 细胞、巨噬细胞和其他免疫细胞也可能受到影响。三级淋巴结构(TLS)是 TME 中的一种独特结构,也是一类包含 T 细胞、B 细胞和其他免疫细胞的聚集体。TLS的成熟度取决于成熟树突状细胞的存在,而TLS的密度则取决于免疫细胞的数量。TLS的成熟度和密度都会影响TME中的抗肿瘤免疫反应。本综述总结了最近关于RT对TLS的影响和作用的研究,包括TLS成分和形成条件的变化以及RT影响TLS和改变TME的机制。RT可促进TLS的成熟和密度,从而改变TME,增强抗肿瘤免疫力。
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引用次数: 0
Epigenetic changes in patients with post-acute COVID-19 symptoms (PACS) and long-COVID: A systematic review. 急性 COVID-19 后症状 (PACS) 和长期 COVID 患者的表观遗传变化:系统综述。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-22 DOI: 10.1017/erm.2024.32
Madhura Shekhar Patil, Emma Richter, Lara Fanning, Jolien Hendrix, Arne Wyns, Laura Barrero Santiago, Jo Nijs, Lode Godderis, Andrea Polli

Background: Up to 30% of people infected with SARS-CoV-2 report disabling symptoms 2 years after the infection. Over 100 persistent symptoms have been associated with Post-Acute COVID-19 Symptoms (PACS) and/or long-COVID, showing a significant clinical heterogeneity. To develop effective, patient-targeted treatment, a better understanding of underlying mechanisms is needed. Epigenetics has helped elucidating the pathophysiology of several health conditions and it might help unravelling inter-individual differences in patients with PACS and long-COVID. As accumulating research is exploring epigenetic mechanisms in PACS and long-COVID, we systematically summarized the available literature on the topic.

Methods: We interrogated five databases (Medline, Embase, Web of Science, Scopus and medXriv/bioXriv) and followed PRISMA and SWiM guidelines to report our results.

Results: Eight studies were included in our review. Six studies explored DNA methylation in PACS and/or long-COVID, while two studies explored miRNA expression in long-COVID associated with lung complications. Sample sizes were mostly small and study quality was low or fair. The main limitation of the included studies was a poor characterization of the patient population that made a homogeneous synthesis of the literature challenging. However, studies on DNA methylation showed that mechanisms related to the immune and the autonomic nervous system, and cell metabolism might be implicated in the pathophysiology of PACS and long-COVID.

Conclusion: Epigenetic changes might help elucidating PACS and long-COVID underlying mechanisms, aid subgrouping, and point towards tailored treatments. Preliminary evidence is promising but scarce. Biological and epigenetic research on long-COVID will benefit millions of people suffering from long-COVID and has the potential to be transferable and benefit other conditions as well, such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). We urge future research to employ longitudinal designs and provide a better characterization of included patients.

背景:多达 30% 的 SARS-CoV-2 感染者在感染 2 年后报告出现致残症状。100多种持续性症状与急性COVID-19后症状(PACS)和/或长期COVID有关,显示出显著的临床异质性。为了开发有效的、针对患者的治疗方法,需要更好地了解潜在的机制。表观遗传学有助于阐明几种健康状况的病理生理学,它可能有助于揭示 PACS 和长期 COVID 患者的个体间差异。随着探索 PACS 和长期 COVID 表观遗传机制的研究不断积累,我们系统地总结了有关这一主题的现有文献:我们查询了五个数据库(Medline、Embase、Web of Science、Scopus 和 medXriv/bioXriv),并遵循 PRISMA 和 SWiM 指南报告结果:结果:八项研究被纳入我们的综述。六项研究探讨了 PACS 和/或 longCOVID 中的 DNA 甲基化,两项研究探讨了与肺部并发症相关的 longCOVID 中 miRNA 的表达。样本量大多较小,研究质量较低或一般。纳入研究的主要局限性在于患者群体的特征描述不清,这使得对文献进行同质化综合具有挑战性。不过,DNA 甲基化研究表明,与免疫和自主神经系统以及细胞代谢有关的机制可能与 PACS 和长 COVID 的病理生理学有关:结论:表观遗传学变化可能有助于阐明 PACS 和长 COVID 的潜在机制,帮助进行亚组划分,并指出有针对性的治疗方法。初步证据很有希望,但数量很少。对长期慢性阻塞性脑损伤的生物学和表观遗传学研究将使数百万长期慢性阻塞性脑损伤患者受益,并有可能推广到其他疾病,如肌痛性脑脊髓炎/慢性疲劳综合征(ME/CFS)。我们敦促未来的研究采用纵向设计,并对纳入的患者进行更好的特征描述。
{"title":"Epigenetic changes in patients with post-acute COVID-19 symptoms (PACS) and long-COVID: A systematic review.","authors":"Madhura Shekhar Patil, Emma Richter, Lara Fanning, Jolien Hendrix, Arne Wyns, Laura Barrero Santiago, Jo Nijs, Lode Godderis, Andrea Polli","doi":"10.1017/erm.2024.32","DOIUrl":"10.1017/erm.2024.32","url":null,"abstract":"<p><strong>Background: </strong>Up to 30% of people infected with SARS-CoV-2 report disabling symptoms 2 years after the infection. Over 100 persistent symptoms have been associated with Post-Acute COVID-19 Symptoms (PACS) and/or long-COVID, showing a significant clinical heterogeneity. To develop effective, patient-targeted treatment, a better understanding of underlying mechanisms is needed. Epigenetics has helped elucidating the pathophysiology of several health conditions and it might help unravelling inter-individual differences in patients with PACS and long-COVID. As accumulating research is exploring epigenetic mechanisms in PACS and long-COVID, we systematically summarized the available literature on the topic.</p><p><strong>Methods: </strong>We interrogated five databases (Medline, Embase, Web of Science, Scopus and medXriv/bioXriv) and followed PRISMA and SWiM guidelines to report our results.</p><p><strong>Results: </strong>Eight studies were included in our review. Six studies explored DNA methylation in PACS and/or long-COVID, while two studies explored miRNA expression in long-COVID associated with lung complications. Sample sizes were mostly small and study quality was low or fair. The main limitation of the included studies was a poor characterization of the patient population that made a homogeneous synthesis of the literature challenging. However, studies on DNA methylation showed that mechanisms related to the immune and the autonomic nervous system, and cell metabolism might be implicated in the pathophysiology of PACS and long-COVID.</p><p><strong>Conclusion: </strong>Epigenetic changes might help elucidating PACS and long-COVID underlying mechanisms, aid subgrouping, and point towards tailored treatments. Preliminary evidence is promising but scarce. Biological and epigenetic research on long-COVID will benefit millions of people suffering from long-COVID and has the potential to be transferable and benefit other conditions as well, such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). We urge future research to employ longitudinal designs and provide a better characterization of included patients.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":"26 ","pages":"e29"},"PeriodicalIF":4.5,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11505605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Advances in multifunctional metal-organic framework (MOF)-based nanoplatforms for cancer starvation therapy. 基于多功能金属有机框架(MOF)的癌症饥饿疗法纳米平台的研究进展。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-14 DOI: 10.1017/erm.2024.28
Jinghan Cai, Yan Xu, Fei Liao

Cancer remains a significant threat to human health today. Even though starvation therapy and other treatment methods have recently advanced to a new level of rapid development in tumour treatment, their limited therapeutic effectiveness and unexpected side effects prevent them from becoming the first option in clinical treatment. With rapid advancement in nanotechnology, the utilization of nanomaterials in therapeutics offers the potential to address the shortcomings in cancer treatment. Notably, multifunctional metal-organic framework (MOF) has been widely employed in cancer therapy due to their customizable shape, adjustable diameter, high porosity, diverse compositions, large specific surface area, high degree of functionalization and strong biocompatibility. This paper reviews the current progress and success of MOF-based multifunctional nanoplatforms for cancer starvation therapy, as well as the prospects and potential barriers for the application of MOF nanoplatforms in cancer starvation therapy.

癌症仍然是当今人类健康的重大威胁。尽管饥饿疗法和其他治疗方法近年来在肿瘤治疗方面迅速发展到一个新水平,但其有限的治疗效果和意想不到的副作用使其无法成为临床治疗的首选。随着纳米技术的快速发展,利用纳米材料进行治疗有望解决癌症治疗中的不足。其中,多功能金属有机框架(MOF)因其形状可定制、直径可调节、孔隙率高、成分多样、比表面积大、功能化程度高、生物相容性强等特点,已被广泛应用于癌症治疗。本文综述了目前基于 MOF 的多功能纳米平台在癌症饥饿疗法中的应用进展和成功案例,以及 MOF 纳米平台在癌症饥饿疗法中的应用前景和潜在障碍。
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引用次数: 0
Thrombocytopenia in dengue infection: mechanisms and a potential application. 登革热感染中的血小板减少症:机制与潜在应用。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-14 DOI: 10.1017/erm.2024.18
Ahmad Suhail Khazali, Waqiyuddin Hilmi Hadrawi, Fatimah Ibrahim, Shatrah Othman, Nurshamimi Nor Rashid

Thrombocytopenia is a common symptom and one of the warning signs of dengue virus (DENV) infection. Platelet depletion is critical as it may lead to other severe dengue symptoms. Understanding the molecular events of this condition during dengue infection is challenging because of the multifaceted factors involved in DENV infection and the dynamics of the disease progression. Platelet levels depend on the balance between platelet production and platelet consumption or clearance. Megakaryopoiesis and thrombopoiesis, two interdependent processes in platelet production, are hampered during dengue infection. Conversely, platelet elimination via platelet activation, apoptosis and clearance processes are elevated. Together, these anomalies contribute to thrombocytopenia in dengue patients. Targeting the molecular events of dengue-mediated thrombocytopenia shows great potential but still requires further investigation. Nonetheless, the application of new knowledge in this field, such as immature platelet fraction analysis, may facilitate physicians in monitoring the progression of the disease.

血小板减少是登革热病毒(DENV)感染的常见症状和预警信号之一。血小板耗竭至关重要,因为它可能导致其他严重的登革热症状。由于登革热病毒感染和疾病进展的动态过程涉及多方面因素,因此了解登革热感染期间这种情况的分子事件具有挑战性。血小板水平取决于血小板生成与血小板消耗或清除之间的平衡。在登革热感染期间,血小板生成的两个相互依存的过程--巨核细胞生成和血栓生成--受到阻碍。相反,通过血小板活化、凋亡和清除过程消除血小板的功能增强。这些异常情况共同导致登革热患者血小板减少。针对登革热介导的血小板减少症分子事件的研究显示出巨大的潜力,但仍需进一步研究。不过,应用这一领域的新知识(如未成熟血小板组分分析)可能有助于医生监测疾病的进展。
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引用次数: 0
Epitranscriptomics and cervical cancer: the emerging role of m6A, m5C and m1A RNA modifications. 表转录组学与宫颈癌:m6A、m5C 和 m1A RNA 修饰的新作用。
IF 4.5 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-08 DOI: 10.1017/erm.2024.20
Akshat D Modi, Hira Zahid, Ashlyn Chase Southerland, Dharmeshkumar M Modi

Cervical cancer (CC), one of the most prevalent and detrimental gynaecologic cancers, evolves through genetic and epigenetic alterations resulting in the promotion of oncogenic activity and dysfunction of tumour-suppressing mechanisms. Despite medical advancement, the prognosis for advanced-stage patients remains extremely low due to high recurrence rates and resistance to existing treatments. Thereby, the search for potential prognostic biomarkers is heightened to unravel new modalities of CC pathogenesis and to develop novel anti-cancer therapies. Epitranscriptomic modifications, reversible epigenetic RNA modifications, regulate various biological processes by deciding RNA fate to mediating RNA interactions. This narrative review provides insight into the cellular and molecular roles of endogenous RNA-editing proteins and their associated epitranscriptomic modifications, especially N6-methyladenosine (m6A), 5-methylcytosine (m5C) and N1-methyladenosine (m1A), in governing the development, progression and metastasis of CC. We discussed the in-depth epitranscriptomic mechanisms underlying the regulation of over 50 RNAs responsible for tumorigenesis, proliferation, migration, invasion, survival, autophagy, stemness, epithelial-mesenchymal transition, metabolism (glucose, lipid, glutamate and glutamine), resistance (drug and radiation), angiogenesis and recurrence of CC. Additionally, we provided a concise overview of the therapeutic potential of targeting the altered expression of endogenous RNA-editing proteins and aberrant deposition of RNA modifications on both coding and non-coding RNAs in CC.

宫颈癌(CC)是发病率最高、危害最大的妇科癌症之一,它通过基因和表观遗传学的改变,导致致癌活性增强和肿瘤抑制机制失调。尽管医疗技术不断进步,但由于复发率高和对现有治疗方法的耐药性,晚期患者的预后仍然极差。因此,寻找潜在的预后生物标志物的工作被提上日程,以揭示 CC 发病的新模式并开发新型抗癌疗法。表观转录组修饰(可逆的表观遗传 RNA 修饰)通过决定 RNA 的命运和介导 RNA 的相互作用来调控各种生物过程。本综述深入探讨了内源性RNA编辑蛋白及其相关表观转录组修饰(尤其是N6-甲基腺苷(m6A)、5-甲基胞嘧啶(m5C)和N1-甲基腺苷(m1A))在调控CC的发生、发展和转移过程中的细胞和分子作用。我们深入探讨了 50 多种 RNA 在调控 CC 的肿瘤发生、增殖、迁移、侵袭、存活、自噬、干性、上皮-间质转化、代谢(葡萄糖、脂质、谷氨酸和谷氨酰胺)、抗药性(药物和辐射)、血管生成和复发方面的表观转录组学机制。此外,我们还简要概述了针对CC中内源性RNA编辑蛋白表达的改变以及编码和非编码RNA上RNA修饰的异常沉积的治疗潜力。
{"title":"Epitranscriptomics and cervical cancer: the emerging role of m<sup>6</sup>A, m<sup>5</sup>C and m<sup>1</sup>A RNA modifications.","authors":"Akshat D Modi, Hira Zahid, Ashlyn Chase Southerland, Dharmeshkumar M Modi","doi":"10.1017/erm.2024.20","DOIUrl":"10.1017/erm.2024.20","url":null,"abstract":"<p><p>Cervical cancer (CC), one of the most prevalent and detrimental gynaecologic cancers, evolves through genetic and epigenetic alterations resulting in the promotion of oncogenic activity and dysfunction of tumour-suppressing mechanisms. Despite medical advancement, the prognosis for advanced-stage patients remains extremely low due to high recurrence rates and resistance to existing treatments. Thereby, the search for potential prognostic biomarkers is heightened to unravel new modalities of CC pathogenesis and to develop novel anti-cancer therapies. Epitranscriptomic modifications, reversible epigenetic RNA modifications, regulate various biological processes by deciding RNA fate to mediating RNA interactions. This narrative review provides insight into the cellular and molecular roles of endogenous RNA-editing proteins and their associated epitranscriptomic modifications, especially <i>N<sup>6</sup></i>-methyladenosine (m<sup>6</sup>A), 5-methylcytosine (m<sup>5</sup>C) and <i>N<sup>1</sup></i>-methyladenosine (m<sup>1</sup>A), in governing the development, progression and metastasis of CC. We discussed the in-depth epitranscriptomic mechanisms underlying the regulation of over 50 RNAs responsible for tumorigenesis, proliferation, migration, invasion, survival, autophagy, stemness, epithelial-mesenchymal transition, metabolism (glucose, lipid, glutamate and glutamine), resistance (drug and radiation), angiogenesis and recurrence of CC. Additionally, we provided a concise overview of the therapeutic potential of targeting the altered expression of endogenous RNA-editing proteins and aberrant deposition of RNA modifications on both coding and non-coding RNAs in CC.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":"26 ","pages":"e20"},"PeriodicalIF":4.5,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11488341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142394923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
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