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The Hox-based positional memory in muscle stem cells. 肌肉干细胞中基于 Hox 的位置记忆。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae059
Ryosuke Okino, Yuki Goda, Yusuke Ono

The skeletal muscle is a contractile tissue distributed throughout the body with various anatomical sizes, shapes and functions. In pathological conditions, such as muscular dystrophy, age-related sarcopenia and cancer cachexia, skeletal muscles are not uniformly affected throughout the body. This region-specific vulnerability cannot be fully explained by known physiological classifications, including muscle fiber types. Accumulating evidence indicates that the expression patterns of topographic homeobox (Hox) genes provide a molecular signature of positional memory, reflecting the anatomical locations and embryonic history of muscles and their associated muscle stem cells in adult mice and humans. Hox-based positional memory is not merely a remnant of embryonic development but is expected to be an intrinsic determinant controlling muscle function because recent studies have shown that aberrant Hox genes affect muscle stem cells. In this review, we discuss the concept of Hox-based positional memory, which may offer a new perspective on the region-specific pathophysiology of muscle disorders.

骨骼肌是一种分布于全身的收缩组织,具有不同的解剖尺寸、形状和功能。在肌肉萎缩症、老年性肌肉疏松症和癌症恶病质等病理情况下,全身骨骼肌受到的影响并不一致。已知的生理分类(包括肌肉纤维类型)无法完全解释这种特定区域的脆弱性。越来越多的证据表明,拓扑同源染色体(Hox)基因的表达模式提供了位置记忆的分子特征,反映了成年小鼠和人类肌肉及其相关肌肉干细胞的解剖位置和胚胎历史。基于 Hox 的位置记忆不仅仅是胚胎发育的残留物,而且有望成为控制肌肉功能的内在决定因素,因为最近的研究表明,异常的 Hox 基因会影响肌肉干细胞。在这篇综述中,我们讨论了基于 Hox 的位置记忆的概念,它可能为肌肉疾病的区域特异性病理生理学提供一个新的视角。
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引用次数: 0
Cutting-edge skin ageing research on tissue stem cell. 关于组织干细胞的尖端皮肤老化研究。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae022
Ryo Ichijo

In developed economies, the growing number of older individuals is a pressing issue. As a result, research progress into ageing has emphasized the significance of staying healthy in one's later years. Stem cells have a fundamental role to play in fostering diverse cell types and necessary processes for tissue repair and regeneration. Stem cells experience the effects of ageing over time, which is caused by their functional deterioration. Changes to stem cells, their niches and signals from other tissues they interact with are crucial factors in the ageing of stem cells. Progress in single-cell RNA sequencing (scRNA-seq) technology has greatly advanced stem cell research. This review examines the mechanisms of stem cell ageing, its impact on health and investigates the potential of stem cell therapy, with a special emphasis on the skin.

在发达经济体中,老年人数量的不断增长是一个紧迫的问题。因此,老龄化研究的进展强调了晚年保持健康的重要性。干细胞在培育多种细胞类型以及组织修复和再生的必要过程中发挥着重要作用。随着时间的推移,干细胞会受到老化的影响,这是由干细胞的功能退化引起的。干细胞及其龛位的变化,以及与之相互作用的其他组织发出的信号,是干细胞老化的关键因素。单细胞RNA测序(scRNA-seq)技术的进步极大地推动了干细胞研究。这篇综述探讨了干细胞老化的机制及其对健康的影响,并研究了干细胞疗法的潜力,特别侧重于皮肤。
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引用次数: 0
Cardiac remodeling: novel pathophysiological mechanisms and therapeutic strategies. 心脏重塑:新的病理生理学机制和治疗策略
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae031
Motohiro Nishida, Xinya Mi, Yukina Ishii, Yuri Kato, Akiyuki Nishimura

Morphological and structural remodeling of the heart, including cardiac hypertrophy and fibrosis, has been considered as a therapeutic target for heart failure for approximately three decades. Groundbreaking heart failure medications demonstrating reverse remodeling effects have contributed significantly to medical advancements. However, nearly 50% of heart failure patients still exhibit drug resistance, posing a challenge to the healthcare system. Recently, characteristics of heart failure resistant to ARBs and β-blockers have been defined, highlighting preserved systolic function despite impaired diastolic function, leading to the classification of heart failure with preserved ejection fraction (HFpEF). The pathogenesis and aetiology of HFpEF may be related to metabolic abnormalities, as evidenced by its mimicry through endothelial dysfunction and excessive intake of high-fat diets. Our recent findings indicate a significant involvement of mitochondrial hyper-fission in the progression of heart failure. This mitochondrial pathological remodeling is associated with redox imbalance, especially hydrogen sulphide accumulation due to abnormal electron leak in myocardium. In this review, we also introduce a novel therapeutic strategy for heart failure from the current perspective of mitochondrial redox-metabolic remodeling.

近三十年来,心脏的形态和结构重塑(包括心脏肥大和纤维化)一直被认为是心力衰竭的治疗目标。具有逆转重塑作用的开创性心衰药物为医学进步做出了巨大贡献。然而,近50%的心衰患者仍表现出耐药性,这给医疗系统带来了挑战。最近,对 ARB 和 β 受体阻滞剂耐药的心衰患者的特征已被确定,这些患者尽管舒张功能受损,但收缩功能仍得到保留,因此被归类为射血分数保留型心衰(HFpEF)。HFpEF 的发病机制和病因可能与新陈代谢异常有关,其通过内皮功能障碍和过量摄入高脂肪饮食而产生的模仿症状就是证明。我们最近的研究结果表明,线粒体过度分裂与心衰的进展有很大关系。这种线粒体病理重塑与氧化还原失衡有关,尤其是心肌中电子泄漏异常导致的硫化氢积累。在这篇综述中,我们还从线粒体氧化还原代谢重塑的角度介绍了一种治疗心衰的新策略。
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引用次数: 0
Sequential post-translational modifications regulate damaged DNA-binding protein DDB2 function. 序列翻译后修饰调节受损 DNA 结合蛋白 DDB2 的功能。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae056
Hidenori Kaneoka, Kazuhiko Arakawa, Yusuke Masuda, Daiki Ogawa, Kota Sugimoto, Risako Fukata, Maasa Tsuge-Shoji, Ken-Ichi Nishijima, Shinji Iijima

Nucleotide excision repair (NER) is a major DNA repair system and hereditary defects in this system cause critical genetic diseases (e.g. xeroderma pigmentosum, Cockayne syndrome and trichothiodystrophy). Various proteins are involved in the eukaryotic NER system and undergo several post-translational modifications. Damaged DNA-binding protein 2 (DDB2) is a DNA damage recognition factor in the NER pathway. We previously demonstrated that DDB2 was SUMOylated in response to UV irradiation; however, its physiological roles remain unclear. We herein analysed several mutants and showed that the N-terminal tail of DDB2 was the target for SUMOylation; however, this region did not contain a consensus SUMOylation sequence. We found a SUMO-interacting motif (SIM) in the N-terminal tail that facilitated SUMOylation. The ubiquitination of a SUMOylation-deficient DDB2 SIM mutant was decreased, and its retention of chromatin was prolonged. The SIM mutant showed impaired NER, possibly due to a decline in the timely handover of the lesion site to XP complementation group C. These results suggest that the SUMOylation of DDB2 facilitates NER through enhancements in ubiquitination.

核苷酸切割修复(NER)是一种主要的 DNA 修复系统,该系统的遗传缺陷会导致严重的遗传疾病(如色素性角化病、科凯恩综合征和毛滴虫体营养不良症)。真核生物的核还原系统涉及多种蛋白质,并经过多种翻译后修饰。损伤 DNA 结合蛋白 2(DDB2)是 NER 途径中的 DNA 损伤识别因子。我们以前曾证实,DDB2 在紫外线照射下会被 SUMOylated,但其生理作用仍不清楚。在此,我们分析了几种突变体,结果表明 DDB2 的 N 端尾部是 SUMO 化的靶标;然而,该区域并不包含共识的 SUMO 化序列。我们在N端尾部发现了一个SUMO-interacting motif (SIM),它能促进SUMO化。SUMO酰化缺陷的DDB2 SIM突变体的泛素化程度降低,在染色质中的保留时间延长。SIM突变体的核还原能力受损,这可能是由于病变位点及时移交给XPC的能力下降所致。这些结果表明,DDB2 的 SUMOylation 可通过增强泛素化来促进 NER。
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引用次数: 0
VP1 of human and murine noroviruses recognizes glycolipid sulfatide via the P domain. 人类和鼠类诺如病毒的 VP1 可通过 P 结构域识别糖脂硫化物。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae051
Bunta Tsukamoto, Yuuki Kurebayashi, Tadanobu Takahashi, Yusuke Abe, Ryohei Ota, Yoshiki Wakabayashi, Anju Nishiie, Akira Minami, Takashi Suzuki, Hideyuki Takeuchi

Noroviruses are a prevalent cause of human viral gastroenteritis, yet the precise mechanisms underlying their infection cycle, particularly their interactions with and entry into cells, remain poorly understood. Human norovirus (HuNoV) primarily targets human small intestinal epithelial cells, within which 3-O-sulfogalactosylceramide (sulfatide) ranks among the most abundant glycosphingolipids (GSLs). While sulfatide involvement in the binding and infection mechanism of several viruses has been documented, its interaction with noroviruses remains underexplored. This study investigated whether noroviruses interact with sulfatide. We found that the recombinant viral capsid protein VP1 of HuNoV (genogroups I and II) and murine norovirus (genogroup V) exhibited robust binding to sulfatide compared with other tested GSLs using enzyme-linked immunosorbent assay, thin-layer chromatography binding assay and real-time quantitative reverse transcription polymerase chain reaction binding assay. VP1 also bound 3-O-sulfated lactosylceramide, which shares the 3-O-sulfated galactose moiety with sulfatide. However, both VP1 and its P domain, identified as the sulfatide-binding domain, exhibited limited binding to structural analogues of sulfatide and other sulfated compounds. These findings suggest a specific recognition of the 3-O-sulfated galactose moiety. Notably, we found that sulfatide is a novel binding target for norovirus particles. Overall, our findings reveal a previously unknown norovirus-sulfatide interaction, proposing sulfatide as a potential candidate for norovirus infection receptors.

诺如病毒是人类病毒性肠胃炎的主要病因,但人们对其感染周期的确切机制,特别是其与细胞的相互作用和进入细胞的机制仍然知之甚少。人类诺如病毒(HuNoV)主要以人类小肠上皮细胞为目标,在这些细胞中,3-O-硫代半乳糖甘油酰胺(硫酰胺)是最丰富的糖磷脂(GSL)之一。虽然已有文献证明硫苷参与了多种病毒的结合和感染机制,但其与诺如病毒的相互作用仍未得到充分探索。本研究调查了诺如病毒是否与硫肽相互作用。通过使用 ELISA、TLC 结合试验和 qRT-PCR 结合试验,我们发现 HuNoV(基因组 I 和 II)和鼠诺如病毒(基因组 V)的重组病毒帽蛋白 VP1 与磺胺类药物的结合力强于其他测试的 GSL。值得注意的是,我们发现硫甙是诺如病毒颗粒的一个新的结合靶标。总之,我们的研究结果揭示了一种以前未知的诺如病毒与硫肽的相互作用,提出硫肽是诺如病毒感染受体的潜在候选物。
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引用次数: 0
Intracellular biliverdin dynamics during ferroptosis. 铁蛋白沉积过程中细胞内胆绿素的动态变化
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-28 DOI: 10.1093/jb/mvae067
Kazuma Nakajima, Hironari Nishizawa, Guan Chen, Shunichi Tsuge, Mie Yamanaka, Machi Kiyohara, Riko Irikura, Mitsuyo Matsumoto, Kozo Tanaka, Rei Narikawa, Kazuhiko Igarashi

Ferroptosis is a cell death mechanism mediated by iron-dependent lipid peroxidation. Although ferroptosis has garnered attention as a cancer-suppressing mechanism, there are still limited markers available for identifying ferroptotic cells or assessing their sensitivity to ferroptosis. The study focused on biliverdin, an endogenous reducing substance in cells, and examined the dynamics of intracellular biliverdin during ferroptosis using a biliverdin-binding cyanobacteriochrome. It was found that intracellular biliverdin decreases during ferroptosis and that this decrease is specific to ferroptosis among different forms of cell death. Furthermore, the feasibility of predicting sensitivity to ferroptosis by measuring intracellular biliverdin was demonstrated using a ferroptosis model induced by the re-expression of the transcription factor BACH1. These findings provide further insight into ferroptosis research and are expected to contribute to the development of cancer therapies that exploit ferroptosis.

铁变态反应是由铁依赖性脂质过氧化介导的一种细胞死亡机制。尽管铁中毒作为一种抑制癌症的机制已引起人们的关注,但目前用于识别铁中毒细胞或评估其对铁中毒敏感性的标记物仍然有限。这项研究的重点是细胞中的内源性还原物质胆绿素,并利用一种与胆绿素结合的蓝细菌色素研究了铁氧化过程中细胞内胆绿素的动态。研究发现,细胞内胆绿素在铁中毒过程中会减少,而且这种减少是不同细胞死亡形式中铁中毒所特有的。此外,利用转录因子 BACH1 的再表达诱导的铁中毒模型,证明了通过测量细胞内胆红素来预测对铁中毒敏感性的可行性。这些发现为铁中毒研究提供了更深入的见解,预计将有助于开发利用铁中毒的癌症疗法。
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引用次数: 0
Absolute quantification of BACH1 and BACH2 transcription factors in B and plasma cells reveals their dynamic changes and unique roles. BACH1 和 BACH2 转录因子在 B 细胞和浆细胞中的绝对定量显示了它们的动态变化和独特作用。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-25 DOI: 10.1093/jb/mvae065
Takeshi Kurasawa, Akihiko Muto, Mitsuyo Matsumoto, Kyoko Ochiai, Kazutaka Murayama, Kazuhiko Igarashi

Changes in the absolute protein amounts of transcription factors are important for regulating gene expression during cell differentiation and in responses to changes in the cellular and extracellular environment. However, few studies have focused on the absolute quantification of mammalian transcription factors. In this study, we established an absolute quantification method for the transcription factors BACH1 and BACH2, which are expressed in B cells and regulated by direct heme binding. The method used purified recombinant proteins as controls in Western blotting and was applied to mouse naïve B cells in the spleen, as well as activated B cells and plasma cells. BACH1 was present in naïve B cells at approximately half the levels of BACH2. In activated B cells, BACH1 decreased compared to naïve B cells, while BACH2 increased. In plasma cells, BACH1 increased back to the same extent as in naïve B cells, while BACH2 was not detected. Their target genes Prdm1 and Hmox1 were highly induced in plasma cells. BACH1 was found to undergo degradation with lower concentrations of heme than BACH2. Therefore, BACH1 and BACH2 are similarly abundant in B cells but differ in heme sensitivity, potentially regulating gene expression differently depending on their heme responsiveness.

转录因子蛋白质绝对量的变化对细胞分化过程中基因表达的调控以及对细胞和细胞外环境变化的反应非常重要。然而,很少有研究关注哺乳动物转录因子的绝对定量。在这项研究中,我们建立了转录因子 BACH1 和 BACH2 的绝对定量方法,它们在 B 细胞中表达,并通过直接血红素结合进行调控。该方法使用纯化的重组蛋白作为 Western 印迹的对照,适用于小鼠脾脏中的幼稚 B 细胞、活化 B 细胞和浆细胞。BACH1 在幼稚 B 细胞中的含量约为 BACH2 的一半。在活化的 B 细胞中,BACH1 比幼稚 B 细胞减少,而 BACH2 增加。在浆细胞中,BACH1 增加的程度与幼稚 B 细胞相同,而 BACH2 则未检测到。它们的靶基因 Prdm1 和 Hmox1 在浆细胞中被高度诱导。与 BACH2 相比,BACH1 在血红素浓度较低时发生降解。因此,BACH1 和 BACH2 在 B 细胞中的含量相似,但对血红素的敏感性不同,它们可能会根据对血红素的敏感性对基因表达进行不同的调控。
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引用次数: 0
BACH to the ferroptosis. BACH to the ferroptosis.
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-24 DOI: 10.1093/jb/mvae064
Fuminori Tokunaga

Ferroptosis is regulated cell death characterized by iron-dependent phospholipid peroxidation, and is closely related to various diseases. System Xc -, a cystine/glutamate antiporter, and glutathione peroxidase 4 (GPX4) are the key molecules in ferroptosis. Erastin and RSL3, known as inhibitors of system Xc - and GPX4, respectively, are commonly used as ferroptosis inducers. BTB and CNC homology 1 (BACH1), a heme-binding transcription repressor, promotes pro-ferroptotic signaling, and therefore, Bach1-deficient cells are resistant to ferroptosis. Irikura et al. constructed Bach1-re-expressing immortalized mouse embryonic fibroblasts (iMEFs) from Bach1-/- mice, which induce ferroptosis simply by the depletion of 2-mercaptoethanol from the culture medium (J. Biochem. 2023; 174:239-252). Transcriptional repression by re-expressed BACH1 induces suppressed glutathione synthesis and increases labile iron. Furthermore, the ferroptosis initiated by BACH1-re-expressing iMEFs is propagated to surrounding cells. Thus, the BACH1-re-expression system is a novel and powerful tool to investigate the cellular basis of ferroptosis.

铁变态反应是以铁依赖性磷脂过氧化为特征的调节性细胞死亡,与多种疾病密切相关。胱氨酸/谷氨酸反转运体 Xc 系统和谷胱甘肽过氧化物酶 4(GPX4)是铁跃变的关键分子。Erastin 和 RSL3 分别被称为 Xc 系统和 GPX4 的抑制剂,常用作铁细胞色素沉着诱导剂。BTB 和 CNC 同源体 1(BACH1)是一种血红素结合转录抑制因子,可促进促铁蛋白沉降的信号转导,因此 Bach1 缺失的细胞对铁蛋白沉降具有抗性。Irikura 等人从 Bach1-/- 小鼠中构建了重新表达 Bach1 的永生化小鼠胚胎成纤维细胞(iMEFs),只需从培养基中去除 2-巯基乙醇就能诱导铁氧化(《生物化学杂志》,2023 年;174:239-252)。重新表达的 BACH1 会抑制谷胱甘肽的合成,并增加可溶性铁。此外,重新表达 BACH1 的 iMEFs 启动的铁变态反应会传播到周围的细胞。因此,BACH1-再表达系统是研究铁变态反应细胞基础的一种新颖而强大的工具。
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引用次数: 0
Transglutaminase mediates the hardening of fish egg envelope produced by duplication of factor XIIIA gene during the evolution of Teleostei. 转谷氨酰胺酶在鱼类进化过程中介导了因子 XIIIA 基因复制产生的鱼卵包膜硬化。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-16 DOI: 10.1093/jb/mvae062
Shigeki Yasumasu, Miyuki Horie, Mayuko Horie, Kodai Sakuma, Chihiro Sato, Hikari Sato, Taiki Nakajima, Tatsuki Nagasawa, Mari Kawaguchi, Ichiro Iuchi

During the fertilization of fish eggs, the hardening of the egg envelope is mediated by transglutaminase (hTGase). After fertilization, TGase undergoes processing. We isolated hTGase from extracts of unfertilized and water-activated rainbow trout eggs. Rainbow trout hTGase (Rt-hTGase) appeared as an 80 kDa protein, and its processed form was 55 kDa. Their N-terminal amino acid sequences were nearly identical, suggesting processing in the C-terminal region. The specific activities were not significantly different, indicating that C-terminal processing does not activate the enzyme itself. We cloned the cDNA by reverse transcription polymerase chain reaction (RT-PCR) using degenerate primers followed by RACE-PCR. The deduced amino acid sequence of the cDNA was similar to that of factor XIII subunit A (FXIIIA). Molecular phylogenetic and gene syntenic analyses clearly showed that hTGase was produced by duplication of FXIIIA during the evolution to Teleostei. The 55 kDa processed form of Rt-hTGase is predominantly composed of an enzyme domain predicted from the amino acid sequence of the cDNA. It is hypothesized that the C-terminal domain of Rt-hTGase binds to egg envelope proteins, and that processing allows the enzyme to move freely within the egg envelope, increasing substrate-enzyme interaction and thereby accelerating hardening.

在鱼卵受精过程中,卵包膜的硬化是由转谷氨酰胺酶(hTGase)介导的。受精后,转谷氨酰胺酶会进行加工。我们从未受精虹鳟鱼卵和水活化虹鳟鱼卵的提取物中分离出了 hTGase。虹鳟鱼 hTGase(Rt-hTGase)呈 80 kDa 蛋白,其加工形式为 55 kDa。它们的 N 端氨基酸序列几乎相同,表明在 C 端区域进行了加工。它们的特异性活性没有明显差异,表明 C 端加工并没有激活酶本身。我们使用变性引物通过反转录聚合酶链反应(RT-PCR)克隆了 cDNA,然后进行了 RACE-PCR。cDNA 的推导氨基酸序列与因子 XIII 亚基 A(FXIIIA)相似。分子系统发育和基因同源分析清楚地表明,hTGase 是由 FXIIIA 在向长尾目进化过程中复制产生的。Rt-hTGase 的 55 kDa 加工形式主要由根据 cDNA 氨基酸序列预测的酶域组成。据推测,Rt-hTGase 的 C 端结构域可与卵包膜蛋白质结合,加工后的酶可在卵包膜内自由移动,增加底物与酶的相互作用,从而加速硬化。
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引用次数: 0
Neutral selection and clonal expansion during the development of colon cancer metastasis. 结肠癌转移发展过程中的中性选择和克隆扩增。
IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-03 DOI: 10.1093/jb/mvae044
Xuelian Lei, Daisuke Yamamoto, Hirotaka Kitamura, Kenji Kita, Noriyuki Inaki, Kazuhiro Murakami, Mizuho Nakayama, Hiroko Oshima, Masanobu Oshima

Intratumour heterogeneity has been shown to play a role in the malignant progression of cancer. The clonal evolution in primary cancer has been well studied, however, that in metastatic tumorigenesis is not fully understood. In this study, we established human colon cancer-derived organoids and investigated clonal dynamics during liver metastasis development by tracking barcode-labelled subclones. Long-term subclone co-cultures showed clonal drift, with a single subclone becoming dominant in the cell population. Interestingly, the selected subclones were not always the same, suggesting that clonal selection was not based on cell intrinsic properties. Furthermore, liver tumours developed by co-transplantation of organoid subclones into the immunodeficient mouse spleen showed a progressive drastic reduction in clonal diversity, and only one or two subclones predominated in the majority of large metastatic tumours. Importantly, selections were not limited to particular subclones but appeared to be random. A trend towards a reduction in clonal diversity was also found in liver metastases of multiple colour-labelled organoids of mouse intestinal tumours. Based on these results, we propose a novel mechanism of metastasis development, i.e. a subclone population of the disseminated tumour cells in the liver is selected by neutral selection during colonization and constitutes large metastatic tumours.

肿瘤内的异质性已被证明在癌症的恶性发展中发挥作用。尽管对原发性癌症中的克隆演化已有深入研究,但对转移性肿瘤发生过程中的克隆演化还不完全了解。在这项研究中,我们建立了人结肠癌器官组织,并通过追踪条形码标记的亚克隆研究了肝转移发展过程中的克隆动态。长期的亚克隆共培养显示出克隆漂移,单个亚克隆在细胞群中占据主导地位。有趣的是,被选择的亚克隆并不总是相同的,这表明克隆选择并非基于细胞的内在特性。此外,将类器官亚克隆共同移植到免疫缺陷小鼠脾脏而形成的肝脏肿瘤显示,克隆多样性逐渐急剧下降,在大多数大的转移性肿瘤中,只有一个或两个亚克隆占主导地位。重要的是,选择并不局限于特定的亚克隆,而似乎是随机的。在小鼠肠道肿瘤的多个彩色标记器官组织的肝转移瘤中也发现了克隆多样性减少的趋势。基于这些结果,我们提出了一种新的转移发展机制,即肝脏中扩散的肿瘤细胞的亚克隆群体在定殖过程中被中性选择,并构成大型转移性肿瘤。
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引用次数: 0
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Journal of biochemistry
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