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

Journal of Cellular Physiology Pub Date : 2025-05-22 DOI:10.1002/jcp.70048

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引用次数: 0

摘要

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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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RETRACTION: MiR-330 Suppresses EMT and Induces Apoptosis by Downregulating HMGA2 in Human Colorectal Cancer

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The above article, published online on June 26, 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.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.

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来源期刊

Journal of Cellular Physiology 生物-生理学

CiteScore

14.70

自引率

0.00%

发文量

256

审稿时长

1 months

期刊介绍： The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.