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New Trick for the Old COP: Cellular Physiology of COPII Condensation in Lipoprotein Secretion 旧COP的新把戏:脂蛋白分泌中COPII缩聚的细胞生理学
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-07-08 DOI: 10.1002/jcp.70061
Xiao Wang, Ke Yang, Xiao-Wei Chen

Products encoded by approximately 30% of the mammalian genome exit the endoplasmic reticulum via the coat complex II (COPII) system en route to their functional destination. Among these cargoes, APOB-containing lipoproteins stand out as abundant and bulky secretory particles with profound implications for human health and diseases. Recent insights into the specialized intracellular itinerary of lipoprotein metabolism and transport not only shed light on longstanding questions of lipid dynamics, but also highlight challenges faced by the COPII machinery in accommodating these complex, unconventional cargoes. Emerging evidence supports that tightly-regulated COPII condensation enables maximal capacity of cargo transport, providing a potential solution tailored for efficient lipoprotein delivery without affecting general protein secretion. This distinction suggests that targeting COPII condensation may provide new therapeutic strategies for lipid-associated diseases. Indeed, recent studies have identified manganese as a key modulator of this process, offering novel insights into its physiological relevance and potential translations.

大约30%的哺乳动物基因组编码的产物通过外壳复合体II (COPII)系统在到达其功能目的地的途中退出内质网。在这些货物中,含apob的脂蛋白作为丰富而庞大的分泌颗粒而突出,对人类健康和疾病具有深远的影响。最近对脂蛋白代谢和运输的细胞内特殊行程的研究不仅揭示了长期存在的脂质动力学问题,而且还强调了COPII机制在适应这些复杂的非常规货物时所面临的挑战。新出现的证据支持,严格调节的COPII冷凝使货物运输能力最大化,提供了一种潜在的解决方案,可在不影响一般蛋白质分泌的情况下有效递送脂蛋白。这一区别表明,靶向COPII缩合可能为脂质相关疾病提供新的治疗策略。事实上,最近的研究已经确定锰是这一过程的关键调节剂,为其生理相关性和潜在的翻译提供了新的见解。
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引用次数: 0
Response to the Letter “Classification and Characterization of Platelet-Rich Fibrin in Regenerative Medicine” 对“再生医学中富血小板纤维蛋白的分类与表征”的回应
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-06-29 DOI: 10.1002/jcp.70059
Sahar Baniameri, Hossein Aminianfar, Niusha Gharehdaghi, Amir-Ali Yousefi-Koma, Sadra Mohaghegh, Hanieh Nokhbatolfoghahaei, Arash Khojasteh
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引用次数: 0
Classification and Characterization of Platelet-Rich Fibrin in Regenerative Medicine 再生医学中富血小板纤维蛋白的分类与表征
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-06-29 DOI: 10.1002/jcp.70060
Shajahan Amitha Banu, Khan Sharun
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引用次数: 0
Dapagliflozin Interrupts Pro-Fibroinflammatory Interleukin 11-Tenascin C Mutual Reinforcement in Fibroblasts by Antagonizing Interleukin-11 Receptor Subunit Alpha 达格列净通过拮抗白介素-11受体亚单位α阻断成纤维细胞中促纤维炎性白介素- 11-Tenascin C的相互强化
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-06-29 DOI: 10.1002/jcp.70052
Yen-Chen Lin, Wei-Jan Chen, Yu-Juei Hsu, Ying-Ju Lai, Cheng-Chin Kuo, Yung-Hsin Yeh

Sodium/glucose cotransporter 2 inhibitors (SGLT2i) protect against heart failure and fibroinflammation with an unclear mechanistic. Recombinant interleukin-11 (IL11) therapy for thrombocytopenia induces heart failure symptoms and signs. Profibrotic IL11 upregulates extracellular matrix (ECM) proteins, whereas pro-inflammatory tenascin-C (TNC) is an ECM-derived alarmin. We hypothesized IL11 upregulated TNC to induce fibroinflammation via Toll-like receptor 4 (TLR4) and prototype SGLT2i dapagliflozin counteracted the effects. We stimulated fibroblasts with IL11 and confirmed TNC upregulation. NADPH oxidase 2 (NOX2) is known to participate in TNC-TLR4 signaling. We treated IL11-stimulated fibroblasts with inhibitors of TLR4 (TLR4i) and NOX2 (NOX2i) and found IL11 induced an imperative profibrotic TNC-TLR4-NOX2 auto-amplification loop. IL11 is known to induce ERK-dependent positive autofeedback. By finding TLR4i and NOX2i inhibited IL11-induced ERK phosphorylation, we suspected IL11-ERK joined TNC-TLR4-NOX2 auto-amplification fibroinflammatory pathway. We stimulated fibroblasts with TNC and found IL11 upregulation. We treated TNC-stimulated fibroblasts with TLR4i, NOX2i, or neutralizing IL11 antibody and confirmed TLR4-NOX2 and IL11 were indispensable for TNC-induced fibrosis. We concluded that IL11-ERK, TNC-TLR4, and NOX2 are interdependent in fibroblasts and together make a positive-feedback loop to sustain fibroinflammation. We checked mRNA expression of relevant proteins from proteinatlas.org and found fibroblasts are overwhelming producers of IL11 and TNC in the heart. IL11 receptor subunit alpha (IL11RA) and TLR4 are highly differentially expressed with the former on cardiomyocytes and the latter on macrophages. We therefore proposed a model of differentially activated IL11RA and TLR4 signaling in response to mutually reinforcing IL11-TNC alarmins, to explain how activated fibroblasts pivotally support fibroinflammatory microenvironment and how danger signals induce cell-type-specific responses. Next, we showed dapagliflozin prevented fibroinflammation induced by IL11 or TNC. Mechanistically, we showed dapagliflozin antagonized IL11RA by molecular docking, fluorescence quenching, and grading-dose IL11-signaling inhibitor cocktails studies. In conclusion, dapagliflozin interrupts pro-fibroinflammatory IL11-TNC bi-alarmin mutual reinforcement in human cardiac fibroblasts by antagonizing IL11RA.

钠/葡萄糖共转运蛋白2抑制剂(SGLT2i)可预防心力衰竭和纤维炎症,其机制尚不清楚。重组白细胞介素-11 (IL11)治疗血小板减少症可诱发心力衰竭症状和体征。促纤维化il - 11上调细胞外基质(ECM)蛋白,而促炎tenascin-C (TNC)是一种来源于ECM的警报蛋白。我们假设IL11通过toll样受体4 (TLR4)上调TNC诱导纤维炎症,而原型SGLT2i达格列净抵消了这一作用。我们用IL11刺激成纤维细胞,证实了TNC的上调。已知NADPH氧化酶2 (NOX2)参与TNC-TLR4信号传导。我们用TLR4 (TLR4i)和NOX2 (NOX2i)抑制剂处理IL11刺激的成纤维细胞,发现IL11诱导了一个必要的促纤维化TNC-TLR4-NOX2自扩增环。已知IL11可诱导erk依赖性的正自反馈。通过发现TLR4i和NOX2i抑制il11诱导的ERK磷酸化,我们怀疑IL11-ERK参与了TNC-TLR4-NOX2自扩增纤维炎症通路。我们用TNC刺激成纤维细胞,发现IL11上调。我们用TLR4i、NOX2i或中和的il - 11抗体处理tnc刺激的成纤维细胞,证实TLR4-NOX2和il - 11对于tnc诱导的纤维化是必不可少的。我们得出结论,IL11-ERK、TNC-TLR4和NOX2在成纤维细胞中相互依赖,并共同形成一个正反馈回路,以维持纤维炎症。我们在proteinatlas.org上检查了相关蛋白的mRNA表达,发现成纤维细胞是心脏中il - 11和TNC的压倒性生产者。il - 11受体亚单位α (IL11RA)和TLR4在心肌细胞和巨噬细胞上的表达存在高度差异。因此,我们提出了一个不同激活的IL11RA和TLR4信号响应相互增强的IL11-TNC警报的模型,以解释激活的成纤维细胞如何关键地支持纤维炎症微环境,以及危险信号如何诱导细胞类型特异性反应。接下来,我们发现达格列净可以预防IL11或TNC诱导的纤维炎症。在机制上,我们通过分子对接、荧光猝灭和分级剂量的il11信号抑制剂鸡尾酒研究表明,达格列净可以拮抗IL11RA。综上所述,达格列净通过拮抗IL11RA阻断了人心脏成纤维细胞中促纤维炎性IL11-TNC双报警蛋白的相互强化。
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引用次数: 0
In Old Mice, Exercise Induces Inflammation and Fibrosis Unless Alk5-Inhibitor and Oxytocin Are Used 在老年小鼠中,运动诱导炎症和纤维化,除非使用alk5抑制剂和催产素
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-06-19 DOI: 10.1002/jcp.70054
Joana Marie C. Cruz, Hayden Yeung, Rana Alzalzalee, Qile Yang, Hannaneh Kabir, Samantha Annaliese McDonough, Xiaoyue Mei, Michael J. Conboy, Irina M. Conboy

Exercise and diet are the best-known methods for attenuating aging-related health decline. However, exercise in older age has diminished gains of strength and agility, and a danger of unrepaired muscle damage. Improving the understanding of age-related differences in response to exercise, our results demonstrate that in old mice, downhill treadmill (eccentric) exercise causes increased influx of CD45+ cells (inflammation) and fibrotic index (fibrosis) in the heart and skeletal muscles. To explain these changes, we identified newly synthesized proteins through bio-orthogonal noncanonical amino acid tagging (BONCAT) and established that exercise exacerbated age-associated protein patterns through a dysregulated transforming growth factor (TGF)-β, Ras/MAPK/PI3Akt, and JAK/STAT pathways. Testing causality, we found that an inhibitor of TGF-β (Alk5 inhibitor, A5i) in combination with the age-diminished peptide oxytocin, previously shown to rejuvenate muscle and brain in sedentary animals, allowed aged mice to exercise without pathologies of skeletal and heart muscles and youthfully restored their de novo proteomes.

运动和节食是最著名的减缓衰老相关的健康衰退的方法。然而,老年人的锻炼会减少力量和敏捷性的增长,并有无法修复的肌肉损伤的危险。我们的研究结果表明,在老年小鼠中,下坡跑步机(偏心)运动导致心脏和骨骼肌中CD45+细胞(炎症)和纤维化指数(纤维化)的流入增加,从而提高了对运动反应的年龄相关差异的理解。为了解释这些变化,我们通过生物正交非规范氨基酸标记(BONCAT)鉴定了新合成的蛋白质,并确定运动通过失调的转化生长因子(TGF)-β、Ras/MAPK/PI3Akt和JAK/STAT通路加剧了年龄相关的蛋白质模式。为了检验因果关系,我们发现TGF-β (Alk5抑制剂,A5i)的抑制剂与衰老肽催产素的结合,先前被证明可以使久坐动物的肌肉和大脑恢复活力,使老年小鼠在没有骨骼肌和心肌病变的情况下运动,并恢复了它们的新生蛋白质组。
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引用次数: 0
The Potential Dual Roles of Metallothionein-1/-2 in Diabetic Osteoarthritis 金属硫蛋白1/ 2在糖尿病性骨关节炎中的潜在双重作用
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-06-16 DOI: 10.1002/jcp.70056
Yu-Ping Su, Rong-Ze Hsieh, Kuo-Ti Peng, Chung-Sheng Shi, Kuo-Chin Huang, Shun-Fu Chang

Osteoarthritis (OA) is increasingly recognized as a chronic inflammatory degenerative joint disease. Recent evidence exhibits a higher prevalence of OA among patients with type II diabetes mellitus (T2DM). Metallothioneins (MTs) are important proteins involved in controlling physiology and pathophysiology. MT-1/MT-2 have been further found their positive correlation with OA progression, but their precise roles need more examination. This study aimed to investigate the role of MT-1/MT-2 in the development of diabetic OA and the underlying mechanisms. Cartilage was collected from patients with OA-only and T2DM-OA, and from rats classified as healthy, T2DM, and T2DM with destabilization of medial meniscus (DMM) surgery. Additionally, a cell model treated with high glucose (HG) or advanced glycation end products (AGEs) was used to investigate underlying mechanisms. Our results revealed that MT-1/MT-2 levels were elevated in cartilage from T2DM-OA patients and rats, as well as in T2DM rats subjected to DMM surgery. Similarly, primary chondrocytes treated with HG and AGE showed increased expression of MT-1/MT-2, with distinct distributions and regulatory mechanisms: (a) MT-1 enhanced MMP and transcription factor activity without affecting their expressions, whereas MT-2 increased both the activity and expression of MMPs and transcription factors; (b) MT-1 reduced IL6/IL8 expression, while MT-2 promoted it. Furthermore, this differential regulation appears to be mediated by BMP2 autocrine stimulation. These findings underscore the dual role of MT-1/MT-2 in simultaneously activating self-repair and degenerative processes, potentially influencing diabetic cartilage pathogenesis. Our study suggests that MT-1/MT-2 may serve as valuable theranostic targets for diabetic OA in future clinical applications.

骨关节炎(OA)越来越被认为是一种慢性炎性退行性关节疾病。最近的证据表明,OA在2型糖尿病(T2DM)患者中发病率更高。金属硫蛋白(MTs)是控制生理和病理生理的重要蛋白。MT-1/MT-2已被进一步发现与OA进展呈正相关,但其确切作用有待进一步研究。本研究旨在探讨MT-1/MT-2在糖尿病性OA发生中的作用及其机制。软骨取自单纯oa和T2DM- oa患者,以及健康、T2DM和T2DM合并内侧半月板失稳手术的大鼠。此外,使用高糖(HG)或晚期糖基化终产物(AGEs)处理的细胞模型来研究潜在的机制。我们的研究结果显示,T2DM- oa患者和大鼠以及接受DMM手术的T2DM大鼠的软骨中MT-1/MT-2水平升高。同样,HG和AGE处理的原代软骨细胞显示MT-1/MT-2的表达增加,其分布和调节机制不同:(a) MT-1增强了MMP和转录因子的活性,但不影响它们的表达,而MT-2增加了MMPs和转录因子的活性和表达;(b) MT-1降低IL6/IL8的表达,而MT-2促进IL6/IL8的表达。此外,这种差异调节似乎是由BMP2自分泌刺激介导的。这些发现强调了MT-1/MT-2在同时激活自我修复和退行性过程中的双重作用,可能影响糖尿病软骨的发病机制。我们的研究表明,MT-1/MT-2可能在未来的临床应用中成为糖尿病性OA的有价值的治疗靶点。
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引用次数: 0
Targeting Heparanase Attenuates Podocyte Injury Induced by Puromycin Aminonucleoside 靶向肝素酶可减轻嘌呤霉素氨基核苷所致足细胞损伤
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-06-10 DOI: 10.1002/jcp.70053
Xing-Yun Huang, Yu-Hsien Lu, Hsiao-Hui Lee

Podocytes are highly specialized glomerular visceral epithelial cells critical for maintaining the structure and function of the glomerular filtration barrier. These cells adhere to the glomerular basement membrane (GBM) and envelop the outer surfaces of the glomerular capillaries to prevent protein leakage during blood ultrafiltration. The GBM is a dense network of extracellular matrix composed of type IV collagen, laminin, nidogen, and heparan sulfate proteoglycans. In this study, we investigated the protective effect of a heparanase inhibitor on puromycin aminonucleoside (PAN)-induced podocyte injury. Our results demonstrate that PAN treatment significantly disrupted the cytoskeletal architecture of cultured podocytes, reducing the formation of focal adhesions and stress fibers. Interdigitating intercellular junctions were replaced by dot-like structures with accumulated filamentous actin. Co-treatment with the heparanase inhibitor PI-88 effectively prevented these PAN-induced cytoskeletal abnormalities. Furthermore, a BSA filtration assay revealed that PI-88 attenuated PAN-induced increases in podocyte monolayer permeability. Taken together, our findings suggest that heparanase inhibition protects against podocyte injury and may represent a potential therapeutic strategy for glomerular diseases.

足细胞是高度特化的肾小球内脏上皮细胞,对维持肾小球滤过屏障的结构和功能至关重要。这些细胞粘附在肾小球基底膜(GBM)上,并包裹在肾小球毛细血管的外表面,以防止血液超滤过程中蛋白质渗漏。GBM是由IV型胶原蛋白、层粘连蛋白、氮素和硫酸肝素蛋白聚糖组成的致密的细胞外基质网络。在这项研究中,我们研究了肝素酶抑制剂对嘌呤霉素氨基核苷(PAN)诱导的足细胞损伤的保护作用。我们的研究结果表明,PAN处理显著破坏了培养足细胞的细胞骨架结构,减少了局灶粘连和应力纤维的形成。交错的细胞间连接被点状结构所取代,这些点状结构含有积累的丝状肌动蛋白。与肝素酶抑制剂PI-88联合治疗可有效预防pan诱导的细胞骨架异常。此外,BSA过滤试验显示,PI-88减弱了pan诱导的足细胞单层通透性的增加。综上所述,我们的研究结果表明,抑制肝素酶可以防止足细胞损伤,并可能代表肾小球疾病的潜在治疗策略。
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引用次数: 0
RETRACTION: Evaluation of Anticancer Effects of Cerium Oxide Nanoparticles on Mouse Fibrosarcoma Cell Line 撤回:氧化铈纳米颗粒对小鼠纤维肉瘤细胞系抗癌作用的评价
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-05-27 DOI: 10.1002/jcp.70051

RETRACTION: E. Nourmohammadi, H. Khoshdel–Sarkarizi, R. Nedaeinia, H. R. Sadeghnia, L. Hasanzadeh, M. Darroudi and R. K. Oskuee, “Evaluation of Anticancer Effects of Cerium Oxide Nanoparticles on Mouse Fibrosarcoma Cell Line,” Journal of Cellular Physiology 234, no. 4 (2019): 4987–4996, https://doi.org/10.1002/jcp.27303.

The above article, published online on 06 September 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation into concerns raised by a third party. The investigation revealed duplication between the L929-Control flow cytometry plot and the L929-Conc30 plot shown in Figure 7b. Furthermore, duplications were identified between the Conc 30 BAX western blot band presented in Figures 9a and the Control BAX western blot band in Figure 9b. These two figures represent different cell lines. An additional duplication was observed between the Control BCL2 band and the Conc 60 BAX band in Figure 9a. The authors provided an explanation and some data, but this was not deemed sufficient. The editors consider the results and conclusions from this study to be substantially compromised. The authors disagree with the retraction.

引用本文:E. Nourmohammadi, H. Khoshdel-Sarkarizi, R. nedainia, H. R. Sadeghnia, L. Hasanzadeh, M. Darroudi, R. K. Oskuee,“氧化铈纳米颗粒对小鼠纤维肉瘤细胞的抗癌作用的评价”,细胞生理学杂志,第234期。4 (2019): 4987-4996, https://doi.org/10.1002/jcp.27303.The上述文章于2018年9月6日在线发表在Wiley在线图书馆(wileyonlinelibrary.com)上,经主编Robert Heath同意撤回;和Wiley期刊有限责任公司。在对第三方提出的问题进行调查后,双方同意撤回论文。研究发现L929-Control流式细胞术图与图7b所示的L929-Conc30图之间存在重复。此外,图9a所示的Conc 30 BAX western blot条带与图9b所示的Control BAX western blot条带之间存在重复。这两个图代表不同的细胞系。在图9a中,在Control BCL2条带和Conc 60 BAX条带之间观察到额外的重复。作者提供了一个解释和一些数据,但这被认为是不够的。编辑认为本研究的结果和结论存在很大的缺陷。作者不同意撤稿。
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引用次数: 0
RETRACTION: Nanos2 Promotes Differentiation of Male Germ Cells Basing on the Negative Regulation of Foxd3 and the Treatment of 5-Azadc and TSA 撤回:Nanos2通过负调控Foxd3及5-Azadc和TSA的作用促进雄性生殖细胞的分化
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-05-26 DOI: 10.1002/jcp.70022

RETRACTION: W. Zhang, Y. Bi, Y. Wang, M. Wang, D. Li, S. Cheng, J. Jin, T. Li, B. Li, and Y. Zhang, “Nanos2 Promotes Differentiation of Male Germ Cells Basing on the Negative Regulation of Foxd3 and the Treatment of 5-Azadc and TSA,” Journal of Cellular Physiology, 234, no. 4 (2019): 3762–3774, https://doi.org/10.1002/jcp.27139.

The above article, published online on 26 August 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, it was brought to the journal's attention that Nanos2 has not been identified in Gallus gallus. Further investigation confirmed that the gene examined in the article was actually Nos2, which encodes nitric oxide synthase 2 (NOS2), a protein with different and unrelated functions from those proposed in the study. Author B. Li stated that she did not directly participate in the experiments conducted for the study and was unaware of its submission. The corresponding author Y. Zhang, on behalf of the remaining co-authors, stated that they mistakenly assumed Nos2, which serves as an alias for Nanos2 in other species, to be homologous to Nanos2 in chickens. This misidentification undermines the study's rationale, methodology, and conclusions. Accordingly, the article is retracted.

引用本文:张伟,毕勇,王艳,王敏,李东东,程生,金军,李涛,李斌,张勇,“Nanos2对雄性生殖细胞分化的调控作用及其对5-Azadc和TSA的治疗作用”,《细胞生理学报》,第34期,no。4 (2019): 3762-3774, https://doi.org/10.1002/jcp.27139.The上述文章于2018年8月26日在线发表在Wiley online Library (wileyonlinelibrary.com)上,经作者、期刊主编Robert Heath同意撤回;和Wiley期刊有限责任公司。由于第三方提出的担忧,已同意撤回。具体来说,引起该杂志注意的是,在Gallus Gallus中尚未发现Nanos2。进一步的研究证实,文章中检测的基因实际上是Nos2,它编码一氧化氮合酶2 (Nos2),这是一种与研究中提出的功能不同且不相关的蛋白质。提交人B. Li说,她没有直接参与为这项研究进行的实验,也不知道该研究的提交。通讯作者Y. Zhang代表其他共同作者表示,他们错误地认为Nos2(在其他物种中作为Nanos2的别名)与鸡中的Nanos2是同源的。这种错误的识别破坏了研究的基本原理、方法和结论。因此,这篇文章被撤回。
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引用次数: 0
RETRACTION: MiR-330 Suppresses EMT and Induces Apoptosis by Downregulating HMGA2 in Human Colorectal Cancer 撤回:MiR-330通过下调HMGA2抑制人结直肠癌EMT并诱导细胞凋亡
IF 4.5 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2025-05-22 DOI: 10.1002/jcp.70048

RETRACTION: Mansoori, B., A. Mohammadi, S. Naghizadeh, et al. 2020. “MiR-330 Suppresses EMT and Induces Apoptosis by Downregulating HMGA2 in Human Colorectal Cancer,” Journal of Cellular Physiology 235, no. 2: 920–931. https://doi.org/10.1002/jcp.29007.

The above article, published online on June 26, 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation by the publisher in response to concerns raised by third parties. Several flaws and inconsistencies have been identified between the described methodology and the presented results. Furthermore, the study's rationale and conclusions drawn are not supported by either the existing literature or the data extracted from The Cancer Genome Atlas (TCGA). Accordingly, the article is retracted as the editors consider its conclusions to be invalid. The authors have been informed of the decision of retraction but not available for a final confirmation.

引用本文:Mansoori, A. Mohammadi, S. Naghizadeh等。2020。MiR-330通过下调HMGA2抑制人类结直肠癌的EMT和诱导细胞凋亡,《细胞生理学杂志》235,第2期。2: 920 - 931。https://doi.org/10.1002/jcp.29007.The以上文章于2019年6月26日在Wiley在线图书馆(wileyonlinelibrary.com)上发表,经主编Robert Heath同意撤回;和Wiley期刊有限责任公司。在出版商对第三方提出的担忧进行调查后,双方同意撤稿。在所描述的方法和提出的结果之间发现了一些缺陷和不一致之处。此外,该研究的基本原理和得出的结论既没有得到现有文献的支持,也没有从癌症基因组图谱(TCGA)中提取的数据。因此,这篇文章被撤回,因为编辑认为其结论无效。作者已被告知撤稿决定,但无法得到最终确认。
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引用次数: 0
期刊
Journal of Cellular Physiology
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