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Initial WNT/β-Catenin or BMP Activation Modulates Inflammatory Response of Mesodermal Progenitors Derived from Human Induced Pluripotent Stem Cells. 初始 WNT/β-Catenin 或 BMP 激活可调节从人类诱导多能干细胞衍生的中胚层祖细胞的炎症反应。
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.3390/cells13211820
Yulia Suzdaltseva, Anastasia Selezneva, Nikita Sergeev, Sergey L Kiselev

Wound healing in adults largely depends on the functional state of multipotent mesenchymal stromal cells (MSCs). Human fetal tissues at the early stages of development are known to heal quickly with a full-quality restoration of the original structure. The differences in the molecular mechanisms that determine the functional activity of mesodermal cells in fetuses and adults remain virtually unknown. Using two independent human induced pluripotent stem cell (iPSC) lines, we examined the effects of the initial WNT and BMP activation on the differentiation of iPSCs via mesodermal progenitors into MSCs and highlighted the functions of these cells that are altered by the proinflammatory microenvironment. The WNT-induced mesoderm commitment of the iPSCs enhanced the expression of paraxial mesoderm (PM)-specific markers, while the BMP4-primed iPSCs exhibited increased levels of lateral mesoderm (LM)-specific genes. The inflammatory status and migration rate of the isogenic iPSC-derived mesoderm cells were assessed via gene expression analysis and scratch assay under the receptor-dependent activation of the proinflammatory IFN-γ or TNF-α signaling pathway. Reduced IDO1 and ICAM1 expression levels were detected in the WNT- and BMP-induced MSC progenitors compared to the isogenic MSCs in response to stimulation with IFN-γ and TNF-α. The WNT- and BMP-induced MSC progenitors exhibited a higher migration rate than isogenic MSCs upon IFN-γ exposure. The established isogenic cellular model will provide new opportunities to elucidate the mechanisms of regeneration and novel therapeutics for wound healing.

成年人的伤口愈合在很大程度上取决于多能间充质基质细胞(MSCs)的功能状态。众所周知,处于发育早期阶段的人类胎儿组织可快速愈合并高质量地恢复原有结构。决定胎儿和成人中胚层细胞功能活性的分子机制差异几乎仍是未知数。我们利用两个独立的人类诱导多能干细胞(iPSC)系,研究了最初的WNT和BMP激活对iPSC经中胚层祖细胞分化为间叶干细胞的影响,并强调了这些细胞的功能会因促炎微环境而改变。WNT诱导的iPSCs中胚层承诺增强了轴旁中胚层(PM)特异性标志物的表达,而BMP4刺激的iPSCs表现出侧中胚层(LM)特异性基因水平的增加。在IFN-γ或TNF-α信号通路的受体依赖性激活下,通过基因表达分析和划痕试验评估了同源iPSC衍生的中胚层细胞的炎症状态和迁移率。与同种间充质干细胞相比,WNT-和BMP诱导的间充质干细胞祖细胞在IFN-γ和TNF-α刺激下IDO1和ICAM1表达水平降低。WNT和BMP诱导的间充质干细胞祖细胞在受到IFN-γ刺激后的迁移率高于同种间充质干细胞。已建立的同源细胞模型将为阐明伤口愈合的再生机制和新型疗法提供新的机会。
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引用次数: 0
Fish Cell Spheroids, a Promising In Vitro Model to Mimic In Vivo Research: A Review. 鱼类细胞球体--模拟体内研究的有望体外模型:综述。
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.3390/cells13211818
Antonio Gómez-Mercader, Luis Monzón-Atienza, Daniel Montero, Jimena Bravo, Félix Acosta

In vitro cell culture systems serve as instrumental platforms for probing biological phenomena and elucidating intricate cellular mechanisms. These systems afford researchers the opportunity to scrutinize cellular responses within a regulated environment, thereby circumventing the ethical and logistical challenges associated with in vivo experimentation. Three-dimensional (3D) cell cultures have emerged as a viable alternative to mimic in vivo environments. Within this context, spheroids are recognized as one of the most straightforward and efficacious models, presenting a promising substitute for conventional monolayer cultures. The application of 3D cultures of fish cells remains limited, focusing mainly on physiological and morphological characterization studies. However, given the capacity of spheroids to emulate in vivo conditions, researchers are exploring diverse applications of these 3D cultures. These include eco-toxicology, immunology, drug screening, endocrinology, and metabolism studies, employing a variety of cell types such as fibroblasts, hepatocytes, embryonic cells, gonadal cells, gastrointestinal cells, and pituitary cells. This review provides a succinct overview, concentrating on the most frequently employed methods for generating fish cell spheroids and their applications to date. The aim is to compile and highlight the significant contributions of these methods to the field and their potential for future research.

体外细胞培养系统是探究生物现象和阐明复杂细胞机制的工具平台。这些系统为研究人员提供了在规范环境中仔细观察细胞反应的机会,从而规避了与体内实验相关的伦理和后勤挑战。三维(3D)细胞培养已成为模拟体内环境的可行替代方法。在此背景下,球形细胞被认为是最直接、最有效的模型之一,有望取代传统的单层培养。鱼类细胞三维培养的应用仍然有限,主要集中在生理和形态特征研究方面。不过,鉴于球形培养物能够模拟体内条件,研究人员正在探索这些三维培养物的多种应用。这些应用包括生态毒理学、免疫学、药物筛选、内分泌学和新陈代谢研究,采用的细胞类型多种多样,如成纤维细胞、肝细胞、胚胎细胞、性腺细胞、胃肠道细胞和垂体细胞。本综述简明扼要地概述了迄今为止最常用的生成鱼细胞球的方法及其应用。目的是汇编和强调这些方法对该领域的重大贡献及其在未来研究中的潜力。
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引用次数: 0
Celastrol-Loaded Hyaluronic Acid/Cancer Cell Membrane Lipid Nanoparticles for Targeted Hepatocellular Carcinoma Prevention. Celastrol Loaded Hyaluronic Acid/Cancer Cell Membrane Lipid Nanoparticles 用于靶向预防肝细胞癌。
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.3390/cells13211819
Peng He, Manshu Zou, Chanjuan Zhang, Yaning Shi, Li Qin

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, and its prevention and treatment face severe challenges. It is crucial to improve the targeting of drugs on tumor cells and tissues. Celastrol (CeT), as an active ingredient of traditional Chinese medicine, possesses strong antitumor effects, especially in triggering apoptosis of HCC. However, due to its toxicity and lack of targeting, its application is greatly limited. HMCLPs, a nano-biomimetic platform carrying CeT with controllable drug release, enhanced targeting, and immunocompatibility, were developed for the first time, which can be used for the treatment of HCC. By utilizing homologous cell membranes and hyaluronic acid (HA), HMCLPs can precisely target tumor regions and release CeT in a controlled manner. Both in vitro and in vivo studies have demonstrated that HMCLPs loaded with CeT significantly increased the accumulation of reactive oxygen species (ROS), induced mitochondrial damage, and triggered apoptosis of HCC cells, resulting in effective treatment with minimal adverse reaction. The development of HMCLPs as a nanocarrier system for CeT delivery offers a promising therapeutic strategy for HCC. This innovative approach improves the targeted delivery and bioavailability of CeT, dramatically induces apoptosis in HCC cells, and exerts its powerful antitumor effects while minimizing systemic toxicity. The present study highlights the potential of combining innovative nanocarriers with powerful natural compounds such as CeT to enhance efficacy and reduce toxicity.

肝细胞癌(HCC)是全球癌症相关死亡的第三大原因,其预防和治疗面临严峻挑战。提高药物对肿瘤细胞和组织的靶向性至关重要。作为中药的一种活性成分,塞拉斯托(Celastrol,CeT)具有很强的抗肿瘤作用,尤其是在引发 HCC 细胞凋亡方面。然而,由于其毒性和缺乏靶向性,其应用受到很大限制。HMCLPs是一种携带CeT的纳米仿生平台,具有药物释放可控、靶向性强、免疫相容性好等特点,可用于治疗HCC。通过利用同源细胞膜和透明质酸(HA),HMCLPs 可精确靶向肿瘤区域并以可控方式释放 CeT。体外和体内研究均表明,含有 CeT 的 HMCLPs 能显著增加活性氧(ROS)的积累,诱导线粒体损伤,并引发 HCC 细胞凋亡,从而实现有效治疗,且不良反应极小。将 HMCLPs 开发成一种用于递送 CeT 的纳米载体系统为治疗 HCC 提供了一种前景广阔的策略。这种创新方法提高了 CeT 的靶向递送和生物利用度,显著诱导 HCC 细胞凋亡,在发挥强大抗肿瘤作用的同时最大限度地降低了全身毒性。本研究强调了将创新纳米载体与 CeT 等强效天然化合物相结合以提高疗效和降低毒性的潜力。
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引用次数: 0
VEGF-Virus Interactions: Pathogenic Mechanisms and Therapeutic Applications. 血管内皮生长因子与病毒的相互作用:致病机制与治疗应用。
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.3390/cells13211815
Cristina Sánchez-Martínez, Esther Grueso, Tania Calvo-López, Jorge Martinez-Ortega, Ana Ruiz, José M Almendral

Many types of viruses directly or indirectly target the vascular endothelial growth factor (VEGF) system, which is a central regulator of vasculogenesis and angiogenesis in physiological homeostasis, causing diverse pathologies. Other viruses have been developed into effective therapeutic tools for VEGF modulation in conditions such as cancer and eye diseases. Some viruses may alter the levels of VEGF in the pathogenesis of respiratory syndromes, or they may encode VEGF-like factors, promoting vascular disruption and angiogenesis to enable viruses' systemic spread. Oncogenic viruses may express interactive factors that perturb VEGF's functional levels or downstream signaling, which increases the neovascularization and metastasis of tumors. Furthermore, many viruses are being developed as therapeutic vectors for vascular pathologies in clinical trials. Major examples are those viral vectors that inhibit the role of VEGF in the neovascularization required for cancer progression; this is achieved through the induction of immune responses, by exposing specific peptides that block signaling or by expressing anti-VEGF and anti-VEGF receptor-neutralizing antibodies. Other viruses have been engineered into effective pro- or anti-angiogenesis multitarget vectors for neovascular eye diseases, paving the way for therapies with improved safety and minimal side effects. This article critically reviews the large body of literature on these issues, highlighting those contributions that describe the molecular mechanisms, thus expanding our understanding of the VEGF-virus interactions in disease and therapy. This could facilitate the clinical use of therapeutic virus vectors in precision medicine for the VEGF system.

血管内皮生长因子(VEGF)是生理平衡中血管生成和血管形成的核心调节因子,许多类型的病毒都直接或间接地以血管内皮生长因子系统为靶标,导致各种病症。其他病毒已被开发成调节血管内皮生长因子的有效治疗工具,用于治疗癌症和眼疾等疾病。一些病毒可能会在呼吸系统综合症的发病过程中改变血管内皮生长因子的水平,也可能编码类似血管内皮生长因子的因子,促进血管破坏和血管生成,使病毒得以全身传播。致癌病毒可能表达交互因子,扰乱血管内皮生长因子的功能水平或下游信号传导,从而增加肿瘤的新生血管和转移。此外,许多病毒正被开发为治疗载体,用于血管病变的临床试验。主要的例子是那些抑制血管内皮生长因子在癌症进展所需的血管新生中发挥作用的病毒载体;这是通过诱导免疫反应、暴露阻断信号转导的特定肽或表达抗血管内皮生长因子和抗血管内皮生长因子受体中和抗体来实现的。其他病毒已被设计成有效的促进或抗血管生成多靶点载体,用于治疗新生血管性眼病,为提高安全性和减少副作用的疗法铺平了道路。本文批判性地回顾了有关这些问题的大量文献,重点介绍了那些描述分子机制的文献,从而拓展了我们对血管内皮生长因子-病毒在疾病和治疗中相互作用的理解。这将促进治疗性病毒载体在血管内皮生长因子系统精准医疗中的临床应用。
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引用次数: 0
NKX3-2 Induces Ovarian Cancer Cell Migration by HDAC6-Mediated Repositioning of Lysosomes and Inhibition of Autophagy. NKX3-2通过HDAC6介导的溶酶体重新定位和抑制自噬诱导卵巢癌细胞迁移
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.3390/cells13211816
Alessandra Ferraresi, Ian Ghezzi, Amreen Salwa, Andrea Esposito, Danny N Dhanasekaran, Ciro Isidoro

Several soluble factors secreted by the stromal cells and cancer cells within the tumor microenvironment facilitate the progression and invasiveness of ovarian cancer. In ovarian cancer cells, lysophosphatidic acid (LPA) modulates the transcriptome profile and promotes cell invasiveness by the downregulation of autophagy. Here, we further elucidate this mechanism by focusing on the molecular and cellular events regulating autophagy. Transcriptomic and Western blotting analyses revealed NKX3-2, a transcriptional factor, to be among the genes hyperexpressed in LPA-stimulated ovarian cancer cells. Bioinformatic analyses revealed that in ovarian cancer patients, the expression of NKX3-2 positively correlates with genes involved in cell motility and migration, while it negatively correlates with macromolecular catabolic pathways. In various ovarian cancer cell lines, NKX3-2 silencing abrogated LPA-induced cell migration. Mechanistically, this effect is linked to the restoration of the HDAC6-mediated relocation of the lysosomes in the para-golgian area, and this results in an increase in autolysosome formation and the overall upregulation of autophagy. Silencing the expression of ATG7 or BECN1, two autophagy genes, rescued the migratory phenotype of the NKX3-2-silenced ovarian cancer cells. Taken together, these data reveal the mechanism by which the LPA-NKX3-2 axis promotes the invasiveness of ovarian cancer cells and supports the possibility of targeting NKX3-2 to reduce the migratory capacity of cancer cells in response to a permissive microenvironment.

肿瘤微环境中的基质细胞和癌细胞分泌的几种可溶性因子促进了卵巢癌的进展和侵袭性。在卵巢癌细胞中,溶血磷脂酸(LPA)通过下调自噬功能调节转录组谱系并促进细胞侵袭性。在这里,我们通过关注调控自噬的分子和细胞事件进一步阐明了这一机制。转录组和 Western 印迹分析显示,NKX3-2(一种转录因子)是 LPA 刺激下卵巢癌细胞高表达的基因之一。生物信息学分析表明,在卵巢癌患者中,NKX3-2的表达与细胞运动和迁移相关基因呈正相关,而与大分子分解途径呈负相关。在各种卵巢癌细胞系中,NKX3-2 的沉默会减弱 LPA 诱导的细胞迁移。从机理上讲,这种效应与 HDAC6 介导的溶酶体在副溶酶体区迁移的恢复有关,这导致自溶酶体形成的增加和自噬的整体上调。抑制 ATG7 或 BECN1(两个自噬基因)的表达可挽救 NKX3-2 沉默卵巢癌细胞的迁移表型。综上所述,这些数据揭示了LPA-NKX3-2轴促进卵巢癌细胞侵袭性的机制,并支持了靶向NKX3-2以降低癌细胞对有利微环境的迁移能力的可能性。
{"title":"NKX3-2 Induces Ovarian Cancer Cell Migration by HDAC6-Mediated Repositioning of Lysosomes and Inhibition of Autophagy.","authors":"Alessandra Ferraresi, Ian Ghezzi, Amreen Salwa, Andrea Esposito, Danny N Dhanasekaran, Ciro Isidoro","doi":"10.3390/cells13211816","DOIUrl":"10.3390/cells13211816","url":null,"abstract":"<p><p>Several soluble factors secreted by the stromal cells and cancer cells within the tumor microenvironment facilitate the progression and invasiveness of ovarian cancer. In ovarian cancer cells, lysophosphatidic acid (LPA) modulates the transcriptome profile and promotes cell invasiveness by the downregulation of autophagy. Here, we further elucidate this mechanism by focusing on the molecular and cellular events regulating autophagy. Transcriptomic and Western blotting analyses revealed NKX3-2, a transcriptional factor, to be among the genes hyperexpressed in LPA-stimulated ovarian cancer cells. Bioinformatic analyses revealed that in ovarian cancer patients, the expression of <i>NKX3-2</i> positively correlates with genes involved in cell motility and migration, while it negatively correlates with macromolecular catabolic pathways. In various ovarian cancer cell lines, NKX3-2 silencing abrogated LPA-induced cell migration. Mechanistically, this effect is linked to the restoration of the HDAC6-mediated relocation of the lysosomes in the para-golgian area, and this results in an increase in autolysosome formation and the overall upregulation of autophagy. Silencing the expression of <i>ATG7</i> or <i>BECN1</i>, two autophagy genes, rescued the migratory phenotype of the NKX3-2-silenced ovarian cancer cells. Taken together, these data reveal the mechanism by which the LPA-NKX3-2 axis promotes the invasiveness of ovarian cancer cells and supports the possibility of targeting NKX3-2 to reduce the migratory capacity of cancer cells in response to a permissive microenvironment.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 21","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction: Svobodova et al. N6-Adenosine Methylation in RNA and a Reduced m3G/TMG Level in Non-Coding RNAs Appear at Microirradiation-Induced DNA Lesions. Cells 2020, 9, 360. 更正:Svobodova 等人,微辐照诱导 DNA 病变中出现的 RNA 中 N6-腺苷甲基化和非编码 RNA 中 m3G/TMG 水平降低。细胞 2020,9,360。
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-04 DOI: 10.3390/cells13211817
Alena Svobodová Kovaříková, Lenka Stixová, Aleš Kovařík, Denisa Komůrková, Soňa Legartová, Paolo Fagherazzi, Eva Bártová

The affiliation number 1, "Institute of Biophysics of the Czech Academy of Sciences, Královopolská 135, 612 65 Brno, Czech Republic" changed its zip code to 612 00 [...].

附属机构 1 "捷克科学院生物物理研究所,Královopolská 135, 612 65 Brno, Czech Republic "的邮政编码改为 612 00 [...].
{"title":"Correction: Svobodova et al. N<sup>6</sup>-Adenosine Methylation in RNA and a Reduced m<sub>3</sub>G/TMG Level in Non-Coding RNAs Appear at Microirradiation-Induced DNA Lesions. <i>Cells</i> 2020, <i>9</i>, 360.","authors":"Alena Svobodová Kovaříková, Lenka Stixová, Aleš Kovařík, Denisa Komůrková, Soňa Legartová, Paolo Fagherazzi, Eva Bártová","doi":"10.3390/cells13211817","DOIUrl":"10.3390/cells13211817","url":null,"abstract":"<p><p>The affiliation number 1, \"Institute of Biophysics of the Czech Academy of Sciences, Královopolská 135, 612 65 Brno, Czech Republic\" changed its zip code to 612 00 [...].</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"13 21","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11545016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Effect of the Acid-Base Imbalance on the Shape and Structure of Red Blood Cells. 酸碱失衡对红细胞形状和结构的影响。
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-03 DOI: 10.3390/cells13211813
Snezhanna Kandrashina, Ekaterina Sherstyukova, Mikhail Shvedov, Vladimir Inozemtsev, Roman Timoshenko, Alexander Erofeev, Maxim Dokukin, Viktoria Sergunova

Red blood cells respond to fluctuations in blood plasma pH by changing the rate of biochemical and physical processes that affect the specific functions of individual cells. This study aimed to analyze the effect of pH changes on red blood cell morphology and structure. The findings revealed that an increase or decrease in pH above or below the physiological level of pH 7.4 results in the transformation of discocytes into echinocytes and causes significant alterations in the membrane, including its roughness, cytoskeleton structure, and the cell's elastic modulus. Furthermore, the study shown a strong connection between critical acidosis and alkalosis with increased intracellular reactive oxygen species production.

红细胞通过改变影响单个细胞特定功能的生化和物理过程的速率来应对血浆 pH 值的波动。本研究旨在分析 pH 值变化对红细胞形态和结构的影响。研究结果表明,pH 值高于或低于生理水平(pH 值为 7.4)会导致盘状细胞转变为棘细胞,并使细胞膜发生显著变化,包括其粗糙度、细胞骨架结构和细胞弹性模量。此外,研究还显示临界酸中毒和碱中毒与细胞内活性氧生成增加之间存在密切联系。
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引用次数: 0
The Crosstalk of Apoptotic and Non-Apoptotic Signaling in CD95 System. CD95 系统中凋亡和非凋亡信号的相互影响
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-03 DOI: 10.3390/cells13211814
Kamil Seyrek, Johannes Espe, Elisabeth Reiss, Inna N Lavrik

The mechanisms of CD95 (Fas/APO-1)-mediated extrinsic apoptotic pathway in cancer cells have been extensively studied. The majority of human cells express CD95, but not all these cells can induce extrinsic apoptosis. Accumulating evidence has shown that CD95 is a multifunctional protein, and its stimulation can also elicit non-apoptotic or even survival signals. It has become clear that under certain cellular contexts, due to the various checkpoints, CD95 activation can trigger both apoptotic and non-apoptotic signals. The crosstalk of death and survival signals may occur at different levels of signal transduction. The strength of the CD95 stimulation, initial levels of anti-apoptotic proteins, and posttranslational modifications of the core DISC components have been proposed to be the most important factors in the life/death decisions at CD95. Successful therapeutic targeting of CD95 signaling pathways will require a better understanding of the crosstalk between CD95-induced apoptotic and cell survival pathways. In this review, in order to gain a systematic understanding of the crosstalk between CD95-mediated apoptosis and non-apoptotic signaling, we will discuss these issues in a step-by-step way.

人们对 CD95(Fas/APO-1)介导的癌细胞外源性凋亡途径的机制进行了广泛的研究。大多数人类细胞都表达 CD95,但并非所有这些细胞都能诱导外源性凋亡。越来越多的证据表明,CD95 是一种多功能蛋白,刺激它也能引起非凋亡甚至生存信号。很明显,在某些细胞环境下,由于各种检查点的作用,CD95 的激活可同时触发凋亡和非凋亡信号。死亡信号和存活信号的串扰可能发生在信号转导的不同层次。CD95 刺激的强度、抗凋亡蛋白的初始水平以及 DISC 核心成分的翻译后修饰被认为是 CD95 决定生死的最重要因素。要想成功地针对 CD95 信号通路进行治疗,就必须更好地了解 CD95 诱导的细胞凋亡和细胞存活通路之间的相互影响。在本综述中,为了系统地了解 CD95 介导的细胞凋亡和非凋亡信号之间的串扰,我们将逐步讨论这些问题。
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引用次数: 0
Regulatory Mechanism of Protein Crotonylation and Its Relationship with Cancer. 蛋白质巴豆酰化的调控机制及其与癌症的关系
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-02 DOI: 10.3390/cells13211812
Siyi Yang, Xinyi Fan, Wei Yu

Crotonylation is a recently discovered protein acyl modification that shares many enzymes with acetylation. However, it possesses a distinct regulatory mechanism and biological function due to its unique crotonyl structure. Since the discovery of crotonylation in 2011, numerous crotonylation sites have been identified in both histones and other proteins. In recent studies, crotonylation was found to play a role in various diseases and biological processes. This paper reviews the initial discovery and regulatory mechanisms of crotonylation, including various writer, reader, and eraser proteins. Finally, we emphasize the relationship of dysregulated protein crotonylation with eight common malignancies, including cervical, prostate, liver, and lung cancer, providing new potential therapeutic targets.

巴豆酰化是最近发现的一种蛋白质酰基修饰,它与乙酰化有许多相同的酶。然而,由于其独特的巴豆酰结构,它具有独特的调控机制和生物功能。自 2011 年发现巴豆酰化以来,已在组蛋白和其他蛋白质中发现了许多巴豆酰化位点。最近的研究发现,巴豆酰化在多种疾病和生物过程中发挥作用。本文回顾了巴豆酰化的初步发现和调控机制,包括各种书写蛋白、阅读蛋白和擦除蛋白。最后,我们强调了蛋白质巴豆酰化失调与八种常见恶性肿瘤(包括宫颈癌、前列腺癌、肝癌和肺癌)的关系,为我们提供了新的潜在治疗靶点。
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引用次数: 0
A Necessary Role for Cyclin D2 Induction During Colon Cancer Progression Mediated by L1. L1 在结肠癌进展过程中诱导细胞周期蛋白 D2 的必要作用
IF 8.3 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2024-11-02 DOI: 10.3390/cells13211810
Arka Saha, Nancy Gavert, Thomas Brabletz, Avri Ben-Ze'ev

The cell adhesion molecule L1CAM (L1), mainly known for its function in brain cells, is a Wnt/β-catenin signaling target gene in colorectal cancer (CRC) cells, where it promotes invasion and liver metastasis. We interrogated which genes are expressed at increased levels in human CRC tissue and induced in CRC cell lines overexpressing L1. We found increased cyclin D2 levels in CRC tissue and LS 174T and HCT 116 human CRC cells overexpressing L1. Increased cyclin D2 in CRC cells was associated with higher proliferation rates, faster motility, tumorigenesis, and liver metastasis. The suppression of cyclin D2 expression by shRNA to cyclin D2 blocked the increase in these cellular properties of L1-expressing cells. The overexpression of cyclin D2 in the absence of L1 also conferred tumorigenic properties similar to L1 expression. The pathways involved in the elevation of cyclin D2 by L1 include NF-κB, Akt, and β-catenin signaling but not the Erk pathway. We found that in a significant percentage of human CRC tissue samples, cyclin D2 is expressed at high levels in the nuclei of cancer cells. At the same time, the adjacent normal mucosa was negative for cyclin D2 staining. The results suggest that the increased cyclin D2 expression by L1 is required to induce proliferative, motile tumor development in CRC tissue and can serve as a diagnostic marker and a target for CRC therapy.

细胞粘附分子 L1CAM(L1)主要因其在脑细胞中的功能而闻名,它是结直肠癌(CRC)细胞中 Wnt/β-catenin 信号转导的靶基因,可促进侵袭和肝转移。我们研究了哪些基因在人类 CRC 组织中表达水平升高,并在过表达 L1 的 CRC 细胞系中被诱导。我们发现,在 CRC 组织以及过表达 L1 的 LS 174T 和 HCT 116 人 CRC 细胞中,细胞周期蛋白 D2 水平升高。CRC 细胞中细胞周期蛋白 D2 的增加与增殖率增高、运动速度加快、肿瘤发生和肝转移有关。通过对细胞周期蛋白 D2 的 shRNA 抑制细胞周期蛋白 D2 的表达,可以阻止 L1 表达细胞的这些细胞特性的增加。在没有L1的情况下,过量表达细胞周期蛋白D2也会产生与L1表达类似的致瘤特性。参与L1使细胞周期蛋白D2升高的途径包括NF-κB、Akt和β-catenin信号转导,但不包括Erk途径。我们发现,在相当比例的人类 CRC 组织样本中,细胞周期蛋白 D2 在癌细胞核中高水平表达。与此同时,邻近的正常粘膜细胞周期蛋白 D2 染色呈阴性。结果表明,L1增加的细胞周期蛋白D2表达是诱导CRC组织中增殖性、运动性肿瘤发展的必要条件,可作为CRC的诊断标志物和治疗靶点。
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引用次数: 0
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