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Bioactivity, hemocompatibility, and inflammatory response of calcium incorporated sulfonated polyether ether ketone on mouse-derived bone marrow cells. 钙结合磺化聚醚醚酮对小鼠骨髓细胞的生物活性、血液相容性和炎症反应
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BSR20232162
Shanmuga Sundar Saravanabhavan, Prabhu Narayanaswamy Venkatesan, Narendranath Jonna, Kamalakannan Vasantha Palaniappan, Zsolt Sarang, Balasubramanian Natesan, Consolato M Sergi

Natural and synthetic polymeric materials, particularly soft and hard tissue replacements, are paramount in medicine. We prepared calcium-incorporated sulfonated polyether-ether ketone (SPEEK) polymer membranes for bone applications. The bioactivity was higher after 21 days of immersion in simulated body fluid (SBF) due to calcium concentration in the membrane. We present a new biomaterial healing system composed of calcium and sulfonated polyether ether ketone (Ca-SPEEK) that can function as a successful biomaterial without causing inflammation when tested on bone marrow cells. The Ca-SPEEK exhibited 13 ± 0.5% clot with low fibrin mesh formation compared to 21 ± 0.5% in SPEEK. In addition, the Ca-SPEEK showed higher protein adsorption than SPEEK membranes. As an inflammatory response, IL-1 and TNF-α in the case of Ca-SPEEK were lower than those for SPEEK. We found an early regulation of IL-10 in the case of Ca-SPEEK at 6 h, which may be attributed to the down-regulation of the inflammatory markers IL-1 and TNF-α. These results evidence the innovative bioactivity of Ca-SPEEK with low inflammatory response, opening venues for bone applications.

天然和合成聚合材料,尤其是软组织和硬组织替代材料,在医学中占有重要地位。我们制备了用于骨骼应用的钙掺杂磺化聚醚醚酮(SPEEK)聚合物膜。 在模拟体液(SBF)中浸泡 21 天后,由于膜中的钙浓度,其生物活性更高。 我们提出了一种由钙和磺化聚醚醚酮(Ca-SPEEK)组成的新型生物材料愈合系统,在对骨髓细胞进行测试时,该系统可作为一种成功的生物材料发挥作用,且不会引起炎症。与 SPEEK 的 21±0.5% 相比,Ca-SPEEK 的凝块率为 13±0.5%,纤维蛋白网的形成率较低。此外,与 SPEEK 膜相比,Ca-SPEEK 的蛋白质吸附率更高。在炎症反应方面,Ca-SPEEK 膜的 IL-1 和 TNF-α 低于 SPEEK 膜。我们发现,钙-SPEEK 膜在 6 小时内对 IL-10 有早期调节作用,这可能是由于下调了炎症标志物 IL-1 和 TNF-。这些结果证明了低炎症反应的 Ca-SPEEK 具有创新的生物活性,为骨应用开辟了道路。
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引用次数: 0
Spatiotemporal regulation of the hepatocyte growth factor receptor MET activity by sorting nexins 1/2 in HCT116 colorectal cancer cells. HCT116 大肠癌细胞中肝细胞生长因子受体 MET 活性受分拣 nexins 1/2 的时空调控。
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BSR20240182
Laiyen Garcia Delgado, Amélie Derome, Samantha Longpré, Marilyne Giroux-Dansereau, Ghenwa Basbous, Christine Lavoie, Caroline Saucier, Jean-Bernard Denault

Cumulative research findings support the idea that endocytic trafficking is crucial in regulating receptor signaling and associated diseases. Specifically, strong evidence points to the involvement of sorting nexins (SNXs), particularly SNX1 and SNX2, in the signaling and trafficking of the receptor tyrosine kinase (RTK) MET in colorectal cancer (CRC). Activation of hepatocyte growth factor (HGF) receptor MET is a key driver of CRC progression. In the present study, we utilized human HCT116 CRC cells with SNX1 and SNX2 genes knocked out to demonstrate that their absence leads to a delay in MET entering early endosomes. This delay results in increased phosphorylation of both MET and AKT upon HGF stimulation, while ERK1/2 (extracellular signal-regulated kinases 1 and 2) phosphorylation remains unaffected. Despite these changes, HGF-induced cell proliferation, scattering, and migration remain similar between the parental and the SNX1/2 knockout cells. However, in the absence of SNX1 and SNX2, these cells exhibit increased resistance to TRAIL-induced apoptosis. This research underscores the intricate relationship between intracellular trafficking, receptor signaling, and cellular responses and demonstrates for the first time that the modulation of MET trafficking by SNX1 and SNX2 is critical for receptor signaling that may exacerbate the disease.

累积的研究结果支持这样一种观点,即内细胞转运在调节受体信号传导和相关疾病中至关重要。具体而言,有确凿证据表明,分选内含蛋白(SNXs),尤其是 SNX1 和 SNX2,参与了结直肠癌(CRC)中受体酪氨酸激酶(RTK)MET 的信号转导和转运。肝细胞生长因子(HGF)受体 MET 的激活是导致 CRC 进展的关键因素。在这项研究中,我们利用敲除了 SNX1 和 SNX2 基因的人 HCT116 CRC 细胞证明,缺少这两个基因会导致 MET 进入早期内体的时间延迟。这种延迟导致 MET 和 AKT 在 HGF 刺激下磷酸化增加,而 ERK1/2(细胞外信号调节激酶 1 和 2)磷酸化不受影响。尽管发生了这些变化,亲代细胞和 SNX1/2 基因敲除细胞在 HGF 诱导的细胞增殖、分散和迁移方面仍然相似。然而,在缺乏 SNX1 和 SNX2 的情况下,这些细胞对 TRAIL 诱导的细胞凋亡表现出更强的抵抗力。这项研究强调了细胞内转运、受体信号转导和细胞反应之间错综复杂的关系,并首次证明了 SNX1 和 SNX2 对 MET 转运的调控对于可能加剧疾病的受体信号转导至关重要。
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引用次数: 0
UCHL1-dependent control of hypoxia-inducible factor transcriptional activity during liver fibrosis. 肝纤维化过程中 UCHL1 对低氧诱导因子转录活性的依赖性控制
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BSR20232147
Amy Collins, Rebecca Scott, Caroline L Wilson, Giuseppe Abbate, Gabrielle B Ecclestone, Adam G Albanese, Demi Biddles, Steven White, Jeremy French, John Moir, Wasfi Alrawashdeh, Colin Wilson, Sanjay Pandanaboyana, John S Hammond, Rohan Thakkar, Fiona Oakley, Jelena Mann, Derek A Mann, Niall S Kenneth

Liver fibrosis is the excessive accumulation of extracellular matrix proteins that occurs in most types of chronic liver disease. At the cellular level, liver fibrosis is associated with the activation of hepatic stellate cells (HSCs) which transdifferentiate into a myofibroblast-like phenotype that is contractile, proliferative and profibrogenic. HSC transdifferentiation induces genome-wide changes in gene expression that enable the cell to adopt its profibrogenic functions. We have previously identified that the deubiquitinase ubiquitin C-terminal hydrolase 1 (UCHL1) is highly induced following HSC activation; however, the cellular targets of its deubiquitinating activity are poorly defined. Here, we describe a role for UCHL1 in regulating the levels and activity of hypoxia-inducible factor 1 (HIF1), an oxygen-sensitive transcription factor, during HSC activation and liver fibrosis. HIF1 is elevated during HSC activation and promotes the expression of profibrotic mediator HIF target genes. Increased HIF1α expression correlated with induction of UCHL1 mRNA and protein with HSC activation. Genetic deletion or chemical inhibition of UCHL1 impaired HIF activity through reduction of HIF1α levels. Furthermore, our mechanistic studies have shown that UCHL1 elevates HIF activity through specific cleavage of degradative ubiquitin chains, elevates levels of pro-fibrotic gene expression and increases proliferation rates. As we also show that UCHL1 inhibition blunts fibrogenesis in a pre-clinical 3D human liver slice model of fibrosis, these results demonstrate how small molecule inhibitors of DUBs can exert therapeutic effects through modulation of HIF transcription factors in liver disease. Furthermore, inhibition of HIF activity using UCHL1 inhibitors may represent a therapeutic opportunity with other HIF-related pathologies.

肝纤维化是大多数慢性肝病中出现的细胞外基质蛋白的过度积累。 在细胞水平上,肝纤维化与肝星状细胞(HSCs)的活化有关,这些细胞转分化为肌成纤维细胞样表型,具有收缩、增殖和嗜碱性。 造血干细胞的转分化会诱导全基因组的基因表达发生变化,从而使细胞具有嗜碱性功能。 在这里,我们描述了 UCHL1 在造血干细胞活化和肝纤维化过程中调节缺氧诱导因子 1(HIF1)(一种对氧敏感的转录因子)的水平和活性的作用。 HIF1 在造血干细胞活化过程中会升高,并促进坏死介质 HIF 靶基因的表达。HIF1α 表达的增加与 HSC 激活时 UCHL1 mRNA 和蛋白质的诱导相关。基因缺失或化学抑制 UCHL1 会降低 HIF1α 的水平,从而削弱 HIF 的活性。此外,我们的机理研究表明,UCHL1 通过特异性裂解降解泛素链提高 HIF 活性,提高促纤维化基因的表达水平并增加增殖率。我们还发现,在临床前三维人体肝纤维化切片模型中,抑制 UCHL1 可减轻纤维化的发生,这些结果证明了小分子 DUB 抑制剂如何通过调节肝病中的 HIF 转录因子发挥治疗作用。 此外,使用 UCHL1 抑制剂抑制 HIF 活性可能是治疗其他 HIF 相关病症的一个机会。
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引用次数: 0
Atox1-cyclin D1 loop activity is critical for survival of tumor cells with inactivated TP53. Atox1-Cyclin D1 环路活动是 TP53 失活肿瘤细胞存活的关键。
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-06-26 DOI: 10.1042/BSR20240389
Oleg A Kuchur, Sofya S Pogodaeva, Anna V Shcherbakova, Segrey A Tsymbal

The search for relevant molecular targets is one of the main tasks of modern tumor chemotherapy. To successfully achieve this, it is necessary to have the most complete understanding of the functioning of a transcriptional apparatus of the cell, particularly related to proliferation. The p53 protein plays an important role in regulating processes such as apoptosis, repair, and cell division, and the loss of its functionality often accompanies various types of tumors and contributes to the development of chemoresistance. Additionally, the proliferative activity of tumor cells is closely related to the metabolism of transition metals. For example, the metallochaperone Atox1 - a copper transporter protein - acts as a transcription activator for cyclin D1, promoting progression through the G1/S phase of the cell cycle. On the other hand, p53 suppresses cyclin D1 at the transcriptional level, thereby these proteins have divergent effects on cell cycle progression. However, the contribution of the interaction between these proteins to cell survival is poorly understood. This work demonstrates that not only exists a positive feedback loop between Atox1 and cyclin D1 but also that the activity of this loop depends on the status of the TP53 gene. Upon inactivation of TP53 in A549 and HepG2 cell lines, the expression of ATOX1 and CCND1 genes is enhanced, and their suppression in these cells leads to pronounced apoptosis. This fundamental observation may be useful in selecting more precise interventions for combined therapy of p53-negative tumors.

寻找相关的分子靶点是现代肿瘤化疗的主要任务之一。要成功实现这一目标,就必须对细胞转录装置的功能有最全面的了解,尤其是与增殖有关的功能。p53 蛋白在调节细胞凋亡、修复和细胞分裂等过程中发挥着重要作用,其功能的丧失往往伴随着各种类型的肿瘤,并导致化疗耐药性的产生。此外,肿瘤细胞的增殖活性与过渡金属的新陈代谢密切相关。例如,金属伴侣 Atox1(一种铜转运蛋白)可作为细胞周期蛋白 D1 的转录激活剂,促进细胞周期 G1/S 阶段的进展。另一方面,p53 在转录水平上抑制细胞周期蛋白 D1,因此这些蛋白对细胞周期的进展具有不同的影响。然而,人们对这些蛋白之间的相互作用对细胞存活的贡献还知之甚少。这项研究表明,Atox1 和细胞周期蛋白 D1 之间不仅存在正反馈环路,而且该环路的活性取决于 TP53 基因的状态。当 A549 和 HepG2 细胞系中的 TP53 失活时,ATOX1 和 CCND1 基因的表达会增强,而它们在这些细胞中的抑制作用会导致细胞明显凋亡。这一基本观察结果可能有助于为 p53 阴性肿瘤的联合治疗选择更精确的干预措施。
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引用次数: 0
Temozolomide resistance mechanisms: unveiling the role of translesion DNA polymerase kappa in glioblastoma spheroids in vitro. 替莫唑胺的抗药性机制:揭示体外胶质母细胞瘤球中转运DNA聚合酶Kappa的作用。
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1042/BSR20230667
Diego Luis Ribeiro, Marcela Teatin Latancia, Izadora de Souza, Abu-Bakr Adetayo Ariwoola, Davi Mendes, Clarissa Ribeiro Reily Rocha, André Van Helvoort Lengert, Carlos Frederico Martins Menck

Temozolomide (TMZ) is the leading therapeutic agent for combating Glioblastoma Multiforme (GBM). Nonetheless, the persistence of chemotherapy-resistant GBM cells remains an ongoing challenge, attributed to various factors, including the translesion synthesis (TLS) mechanism. TLS enables tumor cells to endure genomic damage by utilizing specialized DNA polymerases to bypass DNA lesions. Specifically, TLS polymerase Kappa (Polκ) has been implicated in facilitating DNA damage tolerance against TMZ-induced damage, contributing to a worse prognosis in GBM patients. To better understand the roles of Polκ in TMZ resistance, we conducted a comprehensive assessment of the cytotoxic, antiproliferative, antimetastatic, and genotoxic effects of TMZ on GBM (U251MG) wild-type (WTE) and TLS Polκ knockout (KO) cells, cultivated as three-dimensional (3D) tumor spheroids in vitro. Initial results revealed that TMZ: (i) induces reductions in GBM spheroid diameter (10-200 µM); (ii) demonstrates significant cytotoxicity (25-200 μM); (iii) exerts antiproliferative effects (≤25 μM) and promotes cell cycle arrest (G2/M phase) in Polκ KO spheroids when compared with WTE counterparts. Furthermore, Polκ KO spheroids exhibit elevated levels of cell death (Caspase 3/7) and display greater genotoxicity (53BP1) than WTE following TMZ exposure. Concerning antimetastatic effects, TMZ impedes invadopodia (3D invasion) more effectively in Polκ KO than in WTE spheroids. Collectively, the results suggest that TLS Polκ plays a vital role in the survival, cell death, genotoxicity, and metastatic potential of GBM spheroids in vitro when subjected to TMZ treatment. While the precise mechanisms underpinning this resistance remain elusive, TLS Polκ emerges as a potential therapeutic target for GBM patients.

替莫唑胺(TMZ)是治疗多形性胶质母细胞瘤(GBM)的主要药物。然而,化疗耐药 GBM 细胞的持续存在仍是一个持续的挑战,其原因是多方面的,包括转子合成(TLS)机制。TLS 利用专门的 DNA 聚合酶绕过 DNA 病变,使肿瘤细胞能够承受基因组损伤。具体来说,TLS聚合酶Kappa(Polκ)与促进DNA损伤耐受TMZ诱导的损伤有关,导致GBM患者预后恶化。为了更好地了解 Polκ 在 TMZ 抗性中的作用,我们对 TMZ 对体外培养为三维(3D)肿瘤球的 GBM(U251MG)野生型(WTE)和 TLS Polκ 基因敲除(KO)细胞的细胞毒性、抗增殖性、抗转移性和基因毒性作用进行了全面评估。初步结果显示,TMZ(i)诱导 GBM 球体直径缩小(10-200 μM);(ii)表现出显著的细胞毒性(25-200 μM);(iii)与 WTE 球体相比,Polκ KO 球体具有抗增殖作用(≤ 25 μM),并促进细胞周期停滞(G2/M 期)。此外,与 WTE 相比,Polκ KO 球形细胞暴露于 TMZ 后,细胞死亡水平(Caspase 3/7)升高,并显示出更大的遗传毒性(53BP1)。在抗转移作用方面,TMZ 在 Polκ KO 球形体中比在 WTE 球形体中更有效地阻碍了侵袭(三维侵袭)。总之,这些结果表明,TLS Polκ 在体外 GBM 球形细胞经 TMZ 处理后的存活、细胞死亡、基因毒性和转移潜能方面起着至关重要的作用。虽然这种抗药性的确切机制仍难以捉摸,但TLS Polκ已成为GBM患者的潜在治疗靶点。
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引用次数: 0
Induced pluripotent stem cells in cartilage tissue engineering: a literature review. 软骨组织工程中的诱导多能干细胞:文献综述。
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1042/BSR20232102
Amani Y Owaidah

Osteoarthritis (OA) is a long-term, persistent joint disorder characterized by bone and cartilage degradation, resulting in tightness, pain, and restricted movement. Current attempts in cartilage regeneration are cell-based therapies using stem cells. Multipotent stem cells, such as mesenchymal stem cells (MSCs), and pluripotent stem cells, such as embryonic stem cells (ESCs), have been used to regenerate cartilage. However, since the discovery of human-induced pluripotent stem cells (hiPSCs) in 2007, it was seen as a potential source for regenerative chondrogenic therapy as it overcomes the ethical issues surrounding the use of ESCs and the immunological and differentiation limitations of MSCs. This literature review focuses on chondrogenic differentiation and 3D bioprinting technologies using hiPSCS, suggesting them as a viable source for successful tissue engineering.

Methods: A literature search was conducted using scientific search engines, PubMed, MEDLINE, and Google Scholar databases with the terms 'Cartilage tissue engineering' and 'stem cells' to retrieve published literature on chondrogenic differentiation and tissue engineering using MSCs, ESCs, and hiPSCs.

Results: hiPSCs may provide an effective and autologous treatment for focal chondral lesions, though further research is needed to explore the potential of such technologies.

Conclusions: This review has provided a comprehensive overview of these technologies and the potential applications for hiPSCs in regenerative medicine.

骨关节炎(OA)是一种长期、顽固的关节疾病,其特点是骨和软骨退化,导致紧绷、疼痛和活动受限。目前的软骨再生尝试是使用干细胞的细胞疗法。多能干细胞(如间充质干细胞)和多能干细胞(如胚胎干细胞)已被用于软骨再生。然而,自2007年发现人类诱导多能干细胞(hiPSCs)以来,它被视为软骨再生疗法的潜在来源,因为它克服了围绕使用ESCs的伦理问题以及间充质干细胞的免疫和分化限制。这篇文献综述的重点是使用 hiPSCS 的软骨分化和三维生物打印技术,认为它们是成功组织工程的可行来源:方法:使用科学搜索引擎、PubMed、MEDLINE和google scholar数据库,以 "软骨组织工程 "和 "干细胞 "为关键词进行文献检索,检索已发表的有关使用间充质干细胞、ESC和hiPSCs进行软骨分化和组织工程的文献。结果:hiPSCs可为病灶性软骨损伤提供有效的自体治疗,但仍需进一步研究以探索此类技术的潜力:本综述全面概述了这些技术以及 hiPSCs 在再生医学中的潜在应用。
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引用次数: 0
Loci cg06256735 and cg15815843 in the MFAP5 gene regulatory regions are hypomethylated in varicose veins apparently due to active demethylation. MFAP5基因调控区的cg06256735和cg15815843位点在静脉曲张患者中出现低甲基化,这显然是由于主动去甲基化所致。
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1042/BSR20231938
Mariya A Smetanina, Valeria A Korolenya, Fedor A Sipin, Igor P Oscorbin, Kseniya S Sevostyanova, Konstantin A Gavrilov, Andrey I Shevela, Maxim L Filipenko

Varicose vein disease (VVD) is a common health problem worldwide. Microfibril-associated protein 5 (MFAP5) is one of the potential key players in its pathogenesis. Our previous microarray analysis revealed the cg06256735 and cg15815843 loci in the regulatory regions of the MFAP5 gene as hypomethylated in varicose veins which correlated with its up-regulation. The aim of this work was to validate preliminary microarray data, estimate the level of 5-hydroxymethylcytosine (5hmC) at these loci, and determine the methylation status of one of them in different layers of the venous wall. For this, methyl- and hydroxymethyl-sensitive restriction techniques were used followed by real-time PCR and droplet digital PCR, correspondingly, as well as bisulfite pyrosequencing of +/- oxidized DNA. Our microarray data on hypomethylation at the cg06256735 and cg15815843 loci in whole varicose vein segments were confirmed and it was also demonstrated that the level of 5hmC at these loci is increased in VVD. Specifically, among other layers of the venous wall, tunica (t.) intima is the main contributor to hypomethylation at the cg06256735 locus in varicose veins. Thus, it was shown that hypomethylation at the cg06256735 and cg15815843 loci takes place in VVD, with evidence to suggest that it happens through their active demethylation leading to up-regulation of the MFAP5 gene, and t. intima is most involved in this biochemical process.

静脉曲张疾病(VVD)是全球常见的健康问题。微纤维相关蛋白 5(MFAP5)是其发病机制的潜在关键因素之一。我们之前的微阵列分析发现,在静脉曲张患者中,MFAP5 基因调控区的 cg06256735 和 cg15815843 位点发生了低甲基化,这与该基因的上调有关。这项工作的目的是验证初步的微阵列数据,估算这些位点的 5-羟甲基胞嘧啶(5hmC)水平,并确定其中一个位点在静脉壁不同层的甲基化状态。为此,我们使用了对甲基和羟甲基敏感的限制技术,然后相应地使用了实时 PCR 和液滴数字 PCR 以及 +/- 氧化 DNA 的亚硫酸氢盐热测序技术。我们的微阵列数据证实了曲张静脉全段中 cg06256735 和 cg15815843 位点的低甲基化,还证明了 VVD 中这些位点的 5hmC 水平升高。具体而言,在静脉壁的其他层中,内膜是导致曲张静脉中 cg06256735 基因座低甲基化的主要因素。因此,研究表明,在静脉曲张中,cg06256735 和 cg15815843 基因座发生了低甲基化,有证据表明,这种低甲基化是通过它们的主动去甲基化导致 MFAP5 基因的上调而发生的,而内膜是这一生化过程的主要参与者。
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引用次数: 0
Expression of Concern: Circular RNA S-7 promotes ovarian cancer EMT via sponging miR-641 to upregulate ZEB1 and MDM2. 关注表达:环状 RNA S-7 通过海绵状 miR-641 上调 ZEB1 和 MDM2 促进卵巢癌 EMT。
IF 4.3 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1042/BSR-2020-0825_EOC
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引用次数: 0
Retraction: MicroRNA-223 decreases cell proliferation, migration, invasion and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O1. 撤回:MicroRNA-223 通过靶向叉头盒 O1 降低儿童急性淋巴细胞白血病的细胞增殖、迁移和侵袭,并增强细胞凋亡。
IF 4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1042/BSR-2020-0485_RET
{"title":"Retraction: MicroRNA-223 decreases cell proliferation, migration, invasion and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O1.","authors":"","doi":"10.1042/BSR-2020-0485_RET","DOIUrl":"10.1042/BSR-2020-0485_RET","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"44 5","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141159937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Retraction: MicroRNA-26a reduces synovial inflammation and cartilage injury in osteoarthritis of knee joints through impairing the NF-κB signaling pathway. 撤回:MicroRNA-26a通过损害NF-κB信号通路减轻膝关节骨关节炎的滑膜炎症和软骨损伤
IF 4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-05-29 DOI: 10.1042/BSR-2018-2025_RET
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引用次数: 0
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