RETRACTION: Loss of TET1 Facilitates DLD1 Colon Cancer Cell Migration via H3K27me3-Mediated Down-Regulation of E-Cadherin

IF 4 2区 生物学 Q2 CELL BIOLOGY
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引用次数: 0

Abstract

RETRACTION: Z. Zhou, H.-S. Zhang, Y. Liu, Z.-G. Zhang, G.-Y. Du, H. Li, X.-Y. Yu, and Y.-H. Huang, “Loss of TET1 Facilitates DLD1 Colon Cancer Cell Migration via H3K27me3-Mediated Down-Regulation of E-Cadherin,” Journal of Cellular Physiology 233, no. 2 (2018): 1359–1369, https://doi.org/10.1002/jcp.26012.

The above article, published online on 17 May 2017 in Wiley Online Library (https://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by a third party on PubPeer [1], which revealed inappropriate figure overlaps and suspected image manipulations in Figure 1c among the three columns; Figure 2c partial overlaps within the images shTET1(1) and shTET1(2); and partial overlaps within the images Figure 6b EZH2 and siUTX-1. In addition, concerns were raised about all Western blots in the article, specifically, that the background appears to be very bright due to overly adjusted contrast. Although the corresponding author was responsive and provided a correction of overlapped figures and also shared the original Western blots during the investigation, the Editor-in-Chief and the publisher have decided that a correction could not resolve the concerns raised for this paper. Therefore, the Editor-in-Chief has lost faith in the reliability of the presented results, and the article must be retracted. The authors disagree with the retraction.

References

[1] S. consimilis, “Loss of TET1 facilitates DLD1 colon cancer cell migration via H3K27me3-mediated down-regulation of E-cadherin,” PubPeer, 2024, https://pubpeer.com/publications/FE83376A7CF1DA6D632CA15B7219AE.

撤回:TET1缺失通过h3k27me3介导的E-Cadherin下调促进DLD1结肠癌细胞迁移。
摘编:周志强,h - s。张勇,刘志刚,刘志刚。张,G.-Y。杜,李宏,小勇。Yu和y - h。黄,“TET1缺失通过h3k27me3介导的E-Cadherin下调促进DLD1结肠癌细胞迁移”,细胞生理学杂志,第233期。2 (2018): 1359-1369, https://doi.org/10.1002/jcp.26012.The上述文章于2017年5月17日在线发表在Wiley online Library (https://onlinelibrary.wiley.com/)上,经主编Robert Heath同意撤回;和Wiley期刊有限责任公司。由于第三方对PubPeer b[1]提出的担忧,已同意撤回,该担忧显示图1c中三列之间存在不适当的数字重叠和可疑的图像处理;图2c图像shTET1(1)和shTET1(2)的部分重叠;图6b EZH2和siUTX-1图像的部分重叠。此外,文章中所有的西方斑点都引起了人们的关注,特别是由于过度调整对比度,背景看起来非常明亮。虽然通讯作者在调查过程中做出了回应,并对重叠的数字进行了更正,并分享了原始的西方blots,但主编和出版商认为更正并不能解决本文所提出的担忧。因此,主编已经对所呈现结果的可靠性失去了信心,文章必须被撤回。作者不同意撤稿。参考文献b[1] S. consimilis,“TET1缺失通过h3k27me3介导的E-cadherin下调促进DLD1结肠癌细胞迁移”,PubPeer, 2024, https://pubpeer.com/publications/FE83376A7CF1DA6D632CA15B7219AE。
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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来源期刊
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.
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