transcription factors

转录因子
  • 文章类型: Journal Article
    在神经系统中,替代RNA加工特别普遍,这导致在其他组织中没有发现的数千个转录变体的表达。神经元特异性RNA结合蛋白共转录调节可变剪接,选择性聚腺苷酸化,和RNA编辑,从而塑造神经系统细胞的RNA身份。最近的证据表明,RNA结合蛋白与顺式调节元件如启动子和增强子之间的相互作用在确定神经元特异性表达谱中起作用。这里,我们讨论了转录和RNA加工交叉对话产生独特复杂的神经元转录组的可能机制,专注于替代3'端编队。
    In the nervous system, alternative RNA processing is particularly prevalent, which results in the expression of thousands of transcript variants found in no other tissue. Neuron-specific RNA-binding proteins co-transcriptionally regulate alternative splicing, alternative polyadenylation, and RNA editing, thereby shaping the RNA identity of nervous system cells. Recent evidence suggests that interactions between RNA-binding proteins and cis-regulatory elements such as promoters and enhancers play a role in the determination of neuron-specific expression profiles. Here, we discuss possible mechanisms through which transcription and RNA processing cross-talk to generate the uniquely complex neuronal transcriptome, with a focus on alternative 3\'-end formation.
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  • 文章类型: Journal Article
    与年龄相关的黄斑变性(AMD)作为老年人中央视力丧失的主要原因,引起了全球日益增长的健康问题。
    这项研究的重点是揭示自然杀伤(NK)细胞在AMD中的复杂参与,阐明它们的免疫反应和细胞因子调节作用。
    使用来自基因表达综合数据库的转录组数据,采用单细胞RNA-seq分析。应用高维加权基因共表达网络分析(hdWGCNA)和单细胞调控网络推断和聚类(SCENIC)分析揭示早期AMD患者NK细胞的调控机制。机器学习模型,如随机森林和决策树,用于筛选与AMD相关的hub基因和关键转录因子(TFs)。
    在本研究中确定了不同的细胞簇,特别是T/NK簇,在AMD中观察到NK细胞丰度显著增加。细胞-细胞通讯分析揭示了改变的相互作用,特别是在NK细胞中,表明它们在AMD发病机制中的潜在作用。HdWGCNA强调了绿松石模块,富含炎症相关途径,与NK细胞中的AMD显著相关。场景分析确定了NK细胞调控网络中的关键TF。集线器基因和TFs的整合确定了CREM,FOXP1、IRF1、NFKB2和USF2通过机器学习作为AMD的潜在预测因子。
    这种全面的方法增强了我们对NK细胞动力学的理解,信号改变,和AMD的潜在预测模型。鉴定的TF为分子干预提供了新的途径,并突出了NK细胞与AMD发病机理之间的复杂关系。总的来说,这项研究为推进我们对AMD的理解和管理提供了有价值的见解.
    UNASSIGNED: Age-related Macular Degeneration (AMD) poses a growing global health concern as the leading cause of central vision loss in elderly people.
    UNASSIGNED: This study focuses on unraveling the intricate involvement of Natural Killer (NK) cells in AMD, shedding light on their immune responses and cytokine regulatory roles.
    UNASSIGNED: Transcriptomic data from the Gene Expression Omnibus database were utilized, employing single-cell RNA-seq analysis. High-dimensional weighted gene co-expression network analysis (hdWGCNA) and single-cell regulatory network inference and clustering (SCENIC) analysis were applied to reveal the regulatory mechanisms of NK cells in early-stage AMD patients. Machine learning models, such as random forests and decision trees, were employed to screen hub genes and key transcription factors (TFs) associated with AMD.
    UNASSIGNED: Distinct cell clusters were identified in the present study, especially the T/NK cluster, with a notable increase in NK cell abundance observed in AMD. Cell-cell communication analyses revealed altered interactions, particularly in NK cells, indicating their potential role in AMD pathogenesis. HdWGCNA highlighted the turquoise module, enriched in inflammation-related pathways, as significantly associated with AMD in NK cells. The SCENIC analysis identified key TFs in NK cell regulatory networks. The integration of hub genes and TFs identified CREM, FOXP1, IRF1, NFKB2, and USF2 as potential predictors for AMD through machine learning.
    UNASSIGNED: This comprehensive approach enhances our understanding of NK cell dynamics, signaling alterations, and potential predictive models for AMD. The identified TFs provide new avenues for molecular interventions and highlight the intricate relationship between NK cells and AMD pathogenesis. Overall, this study contributes valuable insights for advancing our understanding and management of AMD.
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  • 文章类型: Journal Article
    背景:棕色脂肪组织(BAT)的激活由于其耗散能量和抵抗心脏代谢疾病(CMD)的能力而受到关注。
    方法:这项研究调查了寒冷暴露对建立的CMD小鼠模型的BAT和肝脏蛋白质组的影响,该模型基于高脂肪,高蔗糖,高胆固醇饮食16周。我们分析了体内能量代谢,并对22°C或5°C维持7天的LdlrKO小鼠的BAT和肝脏进行了非靶向蛋白质组学。
    结果:我们确定了几种失调的途径,miRNA,以及冷暴露Ldlrko小鼠的BAT和肝脏中的转录因子,这些转录因子以前没有在本文中描述过。基于共享下游靶标的调节相互作用网络和配体-受体对的分析将纤维蛋白原α链(FGA)和纤连蛋白1(FN1)确定为响应冷暴露的BAT和肝脏之间的潜在串扰因素。重要的是,编码FGA和FN1基因的遗传变异与人类心脏代谢相关表型和性状相关.
    结论:这项研究描述了关键因素,通路,在冷暴露的CMD小鼠模型中,BAT和肝脏之间的串扰涉及调节网络。这些发现可能为未来的研究提供基础,旨在测试分子介质是否,以及冷暴露时组织适应的调节和信号机制,可能代表心脏代谢紊乱的目标。
    BACKGROUND: Activation of brown adipose tissue (BAT) has gained attention due to its ability to dissipate energy and counteract cardiometabolic diseases (CMDs).
    METHODS: This study investigated the consequences of cold exposure on the BAT and liver proteomes of an established CMD mouse model based on LDL receptor-deficient (LdlrKO) mice fed a high-fat, high-sucrose, high-cholesterol diet for 16 weeks. We analyzed energy metabolism in vivo and performed untargeted proteomics on BAT and liver of LdlrKO mice maintained at 22 °C or 5 °C for 7 days.
    RESULTS: We identified several dysregulated pathways, miRNAs, and transcription factors in BAT and liver of cold-exposed Ldlrko mice that have not been previously described in this context. Networks of regulatory interactions based on shared downstream targets and analysis of ligand-receptor pairs identified fibrinogen alpha chain (FGA) and fibronectin 1 (FN1) as potential crosstalk factors between BAT and liver in response to cold exposure. Importantly, genetic variations in the genes encoding FGA and FN1 have been associated with cardiometabolic-related phenotypes and traits in humans.
    CONCLUSIONS: This study describes the key factors, pathways, and regulatory networks involved in the crosstalk between BAT and the liver in a cold-exposed CMD mouse model. These findings may provide a basis for future studies aimed at testing whether molecular mediators, as well as regulatory and signaling mechanisms involved in tissue adaption upon cold exposure, could represent a target in cardiometabolic disorders.
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  • 文章类型: Journal Article
    背景:越来越多的证据表明,相当比例的疾病相关突变发生在增强子中,基因调控所必需的非编码DNA区域。了解这种变化影响的监管计划的结构和机制可以阐明人类疾病的设备。
    结果:我们从神经分化的七个早期时间点收集表观遗传和基因表达数据集。围绕这个模型系统,我们构建了增强子-启动子相互作用的网络,每个都处于神经诱导的个体阶段。这些网络是一系列丰富分析的基础,通过它,我们证明了它们对各种疾病相关变异的时间动态和富集。我们将Girvan-Newman聚类算法应用于这些网络,以揭示生物学相关的调控子结构。此外,我们展示了使用转录因子过表达和大规模平行报告子试验验证预测的增强子-启动子相互作用的方法。
    结论:我们的研究结果为探索基因调控程序及其在发育过程中的动态提供了一个可推广的框架;这包括研究疾病相关变异对转录网络影响的综合方法。应用于我们网络的技术已经作为计算工具与我们的发现一起发布,E-P-INAnalyzer。我们的程序可以在不同的细胞环境和疾病中使用。
    BACKGROUND: Increasing evidence suggests that a substantial proportion of disease-associated mutations occur in enhancers, regions of non-coding DNA essential to gene regulation. Understanding the structures and mechanisms of the regulatory programs this variation affects can shed light on the apparatuses of human diseases.
    RESULTS: We collect epigenetic and gene expression datasets from seven early time points during neural differentiation. Focusing on this model system, we construct networks of enhancer-promoter interactions, each at an individual stage of neural induction. These networks serve as the base for a rich series of analyses, through which we demonstrate their temporal dynamics and enrichment for various disease-associated variants. We apply the Girvan-Newman clustering algorithm to these networks to reveal biologically relevant substructures of regulation. Additionally, we demonstrate methods to validate predicted enhancer-promoter interactions using transcription factor overexpression and massively parallel reporter assays.
    CONCLUSIONS: Our findings suggest a generalizable framework for exploring gene regulatory programs and their dynamics across developmental processes; this includes a comprehensive approach to studying the effects of disease-associated variation on transcriptional networks. The techniques applied to our networks have been published alongside our findings as a computational tool, E-P-INAnalyzer. Our procedure can be utilized across different cellular contexts and disorders.
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  • 文章类型: Journal Article
    从单细胞RNA测序轨迹推断基因调控网络一直是一个活跃的研究领域,但仍需要方法来识别调控细胞转换的调控因子。我们开发了DREAMIT(在推断轨迹中跨模块表达的动态调节)来注释沿单细胞轨迹分支的转录因子活性,使用关系集合到目标基因。使用代表几种不同组织的基准,以及对造血细胞的ATAC-Seq和Perturb-Seq数据的外部验证,发现该方法比竞争方法具有更高的组织特异性敏感性和特异性.
    Inferring gene regulatory networks from single-cell RNA-sequencing trajectories has been an active area of research yet methods are still needed to identify regulators governing cell transitions. We developed DREAMIT (Dynamic Regulation of Expression Across Modules in Inferred Trajectories) to annotate transcription-factor activity along single-cell trajectory branches, using ensembles of relations to target genes. Using a benchmark representing several different tissues, as well as external validation with ATAC-Seq and Perturb-Seq data on hematopoietic cells, the method was found to have higher tissue-specific sensitivity and specificity over competing approaches.
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  • 文章类型: Journal Article
    形态新奇,或关键创新,有助于生物体的多样化。在植物中,这样的创新之一是合子花的进化,这被认为是促进异花和增加花卉形态多样性。我们从两个Mimulus物种中分离出三个等位基因突变体,这些突变体显示出改变的花对称性,并将因果基因鉴定为拟南芥BLADE-ON-PETIOLE的直系同源物。我们发现MlBOP和MlCYC2A物理相互作用,并且该BOP-CYC相互作用模块在被子植物中高度保守。此外,MlBOP自泛素化并抑制MlCYC2A自激活。MlCYC2A,反过来,阻碍MlBOP泛素化。因此,MlBOP和MlCYC2A之间的这种分子拉锯战微调了MlCYC2A的表达,有助于花的双侧对称性的形成,被子植物进化的一个关键特征.
    Morphological novelties, or key innovations, are instrumental to the diversification of the organisms. In plants, one such innovation is the evolution of zygomorphic flowers, which is thought to promote outcrossing and increase flower morphological diversity. We isolated three allelic mutants from two Mimulus species displaying altered floral symmetry and identified the causal gene as the ortholog of Arabidopsis BLADE-ON-PETIOLE. We found that MlBOP and MlCYC2A physically interact and this BOP-CYC interaction module is highly conserved across the angiosperms. Furthermore, MlBOP self-ubiquitinates and suppresses MlCYC2A self-activation. MlCYC2A, in turn, impedes MlBOP ubiquitination. Thus, this molecular tug-of-war between MlBOP and MlCYC2A fine-tunes the expression of MlCYC2A, contributing to the formation of bilateral symmetry in flowers, a key trait in angiosperm evolution.
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  • 文章类型: Journal Article
    植物免疫的组成部分是通过特定转录因子的协同作用进行转录重编程,这些转录因子通过募集或释放RNA聚合酶II(PolII)来激活或抑制基因。通过与包括转录因子IIB(TFIIB)在内的一组通用转录因子结合,在启动子处将PolII组装成PolII全酶以激活转录。与其他真核生物不同,植物有一个TFIIB相关蛋白大家族,在拟南芥中有15个成员,包括几种植物特异性TFIIB相关蛋白(BRP)。分子遗传分析揭示了一些BRPs在植物生殖过程中的重要作用。在这项研究中,我们报道了BRP蛋白家族的创始成员BRP1的拟南芥基因敲除突变体,生长发育正常,但是对细菌病原体丁香假单胞菌高度敏感。brp1突变体的敏感性增强与水杨酸(SA)生物合成基因异协调酸合成酶1(ICS1)和SA反应性致病基因相关(PR)基因的表达降低有关。在brp1突变体中,病原体诱导的SA积累减少,外源SA挽救了brp1突变体对细菌病原体的抗性。在未感染的植物中,BRP1主要与质体相关,但病原体感染会诱导其在细胞核中的积累。BRP1在植物细胞中充当转录激活因子,并与ICS1的启动子结合。这些结果共同表明BRP1是功能上特化的转录因子,其响应于病原体感染而在细胞核中逐渐积累以促进防御基因表达。
    An integral part of plant immunity is transcription reprogramming by concerted action of specific transcription factors that activate or repress genes through recruitment or release of RNA polymerase II (Pol II). Pol II is assembled into Pol II holoenzyme at the promoters through association with a group of general transcription factors including transcription factor IIB (TFIIB) to activate transcription. Unlike other eukaryotic organisms, plants have a large family of TFIIB-related proteins with 15 members in Arabidopsis including several plant-specific TFIIB-related proteins (BRPs). Molecular genetic analysis has revealed important roles of some BRPs in plant reproductive processes. In this study, we report that Arabidopsis knockout mutants for BRP1, the founding member of the BRP protein family, were normal in growth and development, but were hypersusceptible to the bacterial pathogen Psuedomonas syringae. The enhanced susceptibility of the brp1 mutants was associated with reduced expression of salicylic acid (SA) biosynthetic gene ISOCHORISMATE SYNTHASE 1 (ICS1) and SA-responsive PATHOGENESIS-RELATED (PR) genes. Pathogen-induced SA accumulation was reduced in the brp1 mutants and exogenous SA rescued the brp1 mutants for resistance to the bacterial pathogen. In uninfected plants, BRP1 was primarily associated with the plastids but pathogen infection induced its accumulation in the nucleus. BRP1 acted as a transcription activator in plant cells and binded to the promoter of ICS1. These results collectively indicate that BRP1 is a functionally specialized transcription factor that increasingly accumulates in the nucleus in response to pathogen infection to promote defense gene expression.
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  • 文章类型: Journal Article
    植物激素相关转录因子(TFs)是植物发育的关键调控因子,对气候变化等环境压力的反应,病原体,和害虫。这些TFs通常在高等植物中表现出遗传冗余的家族,并且受到不同植物激素之间复杂的串扰机制的影响。这些性质使得在许多情况下难以分析和控制它们。在这项研究中,我们引入了一种化学抑制剂来操纵植物激素相关的TFs,关注茉莉酸(JA)和乙烯(ET)信号通路,与关键TFsMYC2/3/4和EIN3/EIL1。这项研究表明,JAZ10CMID,参与两种TFs脱敏的阻遏物的结合域,是在没有结合伴侣的情况下的内在无序区域。已经基于这种相互作用设计了化学抑制剂以选择性地抑制MYCTF,同时使EIN3/EIL1不受影响。这种肽抑制剂有效地破坏MYC介导的反应,同时激活EIN3介导的反应,并成功地解开拟南芥中JA和ET信号之间的串扰。此外,设计的肽抑制剂还显示选择性地抑制MpMYC的活性,Marchantiapolymora中AtMYC的直系同源物,证明了它在不同植物物种中的适用性。这强调了将肽抑制剂用于特定TFs以阐明非模型植物中的激素串扰机制而无需遗传操作的潜力。这种用于无序结构的化学固定的设计概念有望限制原始的多个结合伴侣,并在化学生物学研究中提供有用的化学工具。
    Plant hormone-related transcription factors (TFs) are key regulators of plant development, responses to environmental stress such as climate changes, pathogens, and pests. These TFs often function as families that exhibit genetic redundancy in higher plants, and are affected by complex crosstalk mechanisms between different plant hormones. These properties make it difficult to analyze and control them in many cases. In this study, we introduced a chemical inhibitor to manipulate plant hormone-related TFs, focusing on the jasmonate (JA) and ethylene (ET) signaling pathways, with the key TFs MYC2/3/4 and EIN3/EIL1. This study revealed that JAZ10CMID, the binding domain of the repressor involved in the desensitization of both TFs, is an intrinsically disordered region in the absence of binding partners. Chemical inhibitors have been designed based on this interaction to selectively inhibit MYC TFs while leaving EIN3/EIL1 unaffected. This peptide inhibitor effectively disrupts MYC-mediated responses while activating EIN3-mediated responses and successfully uncouples the crosstalk between JA and ET signaling in Arabidopsis thaliana. Furthermore, the designed peptide inhibitor was also shown to selectively inhibit the activity of MpMYC, an ortholog of AtMYC in Marchantia polymorpha, demonstrating its applicability across different plant species. This underscores the potential of using peptide inhibitors for specific TFs to elucidate hormone crosstalk mechanisms in non-model plants without genetic manipulation. Such a design concept for chemical fixation of the disordered structure is expected to limit the original multiple binding partners and provide useful chemical tools in chemical biology research.
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  • 文章类型: Journal Article
    背景:中国樱桃[Cerasuspseudocerasus(Lindl。)G.Don](syn.李pseudocerasLindl。)是一种经济上重要的结果樱桃品种,具有多种诱人的颜色,从最亮的黄色到最暗的黑色紫色。然而,参与花色苷生物合成的MYB转录因子在中国樱桃果实颜色变化的基础上仍然未知。
    结果:在这项研究中,我们通过全基因组鉴定鉴定了中国樱桃的R2R3-MYB基因家族,并将其与10个玫瑰科亲属和拟南芥的基因进行了比较。共有1490个R2R3-MYB被分为43个亚家族,其中包括29个亚科,同时含有玫瑰科MYBs和AtMYBs。一个亚科(S45)仅包含玫瑰科MYBs,而三个亚家族(S12,S75和S77)仅包含AtMYB。不同物种之间相同亚科中基因数量的差异以及某些物种中某些亚科的缺失表明,中国樱桃及其近缘种MYB基因家族中的物种特异性扩增。分段和串联重复事件主要促进了中国樱桃R2R3-CpMYB的扩展。复制的基因对在复制事件后的进化过程中经历了纯化选择。系统发育关系和转录谱显示,CpMYB10和CpMYB4参与了中国樱桃果实花色苷生物合成的调控。表达模式,瞬时过表达和VIGS结果证实CpMYB10促进了果皮中花青素的积累,而CpMYB4作为阻遏物,抑制樱桃花色苷的生物合成.
    结论:本研究对中国樱桃和玫瑰科近缘种的R2R3-MYB基因家族进行了全面系统的分析,并确定了两个监管机构,CpMYB10和CpMYB4参与樱桃花色苷的合成.这些结果有助于开发和利用中国樱桃花色苷的潜在功能。
    BACKGROUND: Chinese cherry [Cerasus pseudocerasus (Lindl.) G.Don] (syn. Prunus pseudocerasus Lindl.) is an economically important fruiting cherry species with a diverse range of attractive colors, spanning from the lightest yellow to the darkest black purple. However, the MYB transcription factors involved in anthocyanin biosynthesis underlying fruit color variation in Chinese cherry remain unknown.
    RESULTS: In this study, we characterized the R2R3-MYB gene family of Chinese cherry by genome-wide identification and compared it with those of 10 Rosaceae relatives and Arabidopsis thaliana. A total of 1490 R2R3-MYBs were classified into 43 subfamilies, which included 29 subfamilies containing both Rosaceae MYBs and AtMYBs. One subfamily (S45) contained only Rosaceae MYBs, while three subfamilies (S12, S75, and S77) contained only AtMYBs. The variation in gene numbers within identical subfamilies among different species and the absence of certain subfamilies in some species indicated the species-specific expansion within MYB gene family in Chinese cherry and its relatives. Segmental and tandem duplication events primarily contributed to the expansion of Chinese cherry R2R3-CpMYBs. The duplicated gene pairs underwent purifying selection during evolution after duplication events. Phylogenetic relationships and transcript profiling revealed that CpMYB10 and CpMYB4 are involved in the regulation of anthocyanin biosynthesis in Chinese cherry fruits. Expression patterns, transient overexpression and VIGS results confirmed that CpMYB10 promotes anthocyanin accumulation in the fruit skin, while CpMYB4 acts as a repressor, inhibiting anthocyanin biosynthesis of Chinese cherry.
    CONCLUSIONS: This study provides a comprehensive and systematic analysis of R2R3-MYB gene family in Chinese cherry and Rosaceae relatives, and identifies two regulators, CpMYB10 and CpMYB4, involved in anthocyanin biosynthesis in Chinese cherry. These results help to develop and utilize the potential functions of anthocyanins in Chinese cherry.
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  • 文章类型: Journal Article
    透明细胞卵巢癌(CCOC)的细胞起源,卵巢癌的主要组织学亚型仍然难以捉摸。这里,我们探索了候选细胞来源,并使用整合的基因组/表观基因组分析鉴定了分子亚型.我们进行了全外显子组测序,微阵列,根据原始诊断,对78份CCOC样本进行DNA甲基化阵列。结果表明,ARID1A和/或PIK3CA突变与DNA修复相关基因是相互排斥的,包括TP53、BRCA1和ATM。CCOC和其他卵巢癌(n=270)与输卵管正常组织的聚集,卵巢表面上皮,子宫内膜上皮,和盆腔腹膜间皮(PPM)在甲基化阵列中显示主要CCOC亚型(具有ARID1A和/或PIK3CA突变)与PPM-lile簇相关(n=64)。该簇被细分为三个簇:(1)错配修复(MMR)缺乏肿瘤突变负荷高(n=2),(2)ARID1A的改变(n=51),和(3)ARID1A野生型(n=11)。其余样品(n=14)被细分为(4)卵巢表面上皮样(n=11)和(5)输卵管样(被认为是高级浆液性组织型;n=3)。其中,亚型(1-3)和其他(4和5)被发现与免疫反应特征和上皮-间质转化有关,分别。这些结果有助于将CCOC分层为生物亚型。
    The cellular origin of clear cell ovarian carcinoma (CCOC), a major histological subtype of ovarian carcinoma remains elusive. Here, we explored the candidate cellular origin and identify molecular subtypes using integrated genomic/epigenomic analysis. We performed whole exome-sequencing, microarray, and DNA methylation array in 78 CCOC samples according to the original diagnosis. The findings revealed that ARID1A and/or PIK3CA mutations were mutually exclusive with DNA repair related genes, including TP53, BRCA1, and ATM. Clustering of CCOC and other ovarian carcinomas (n = 270) with normal tissues from the fallopian tube, ovarian surface epithelium, endometrial epithelium, and pelvic peritoneum mesothelium (PPM) in a methylation array showed that major CCOC subtypes (with ARID1A and/or PIK3CA mutations) were associated with the PPM-lile cluster (n = 64). This cluster was sub-divided into three clusters: (1) mismatch repair (MMR) deficient with tumor mutational burden-high (n = 2), (2) alteration of ARID1A (n = 51), and (3) ARID1A wild-type (n = 11). The remaining samples (n = 14) were subdivided into (4) ovarian surface epithelium-like (n = 11) and (5) fallopian tube-like (considered as high-grade serous histotype; n = 3). Among these, subtypes (1-3) and others (4 and 5) were found to be associated with immunoreactive signatures and epithelial-mesenchymal transition, respectively. These results contribute to the stratification of CCOC into biological subtypes.
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