RETRACTION: Promotion of Cell Autophagy and Apoptosis in Cervical Cancer by Inhibition of Long Noncoding RNA LINC00511 via Transcription Factor RXRA-regulated PLD1

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
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引用次数: 0

Abstract

RETRACTION: Y. Shi, M. Liu, Y. Huang, J. Zhang, and L. Yin, “Promotion of Cell Autophagy and Apoptosis in Cervical Cancer by Inhibition of Long Noncoding RNA LINC00511 via Transcription Factor RXRA-regulated PLD1,” Journal of Cellular Physiology 235, no. 10 (2020): 6592-6604. https://doi.org/10.1002/jcp.29529.

The above article, published online on 17 February 2020 in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. A third party reported that images shared overlapping sections in Figure 5D in this article, and this duplication was confirmed by the publisher. The third party also reported that the tumor measurement ruler used in Figure 5 A is identical to the ruler used in the figures of previously published articles from different authors, each of which describes a different scientific context (Chen, et al. 2019 [https://doi.org/10.1002/jcp.28911]) and (Feng, et al. 2019 [https://doi.org/10.1186/s13287-022-02841-z]). The use of the identical ruler in the figures of different articles from unrelated research groups at different institutions puts in doubt the veracity of the data reported. The authors did not respond to an inquiry by the publisher. The retraction has been agreed on because the evidence of image duplication within this article, as well as unexplained duplication of image elements and equipment with other experiments by different authors, fundamentally compromises the conclusions reported in this article. The authors did not respond to our notice regarding the retraction.

通过转录因子rxra调控的PLD1抑制长链非编码RNA LINC00511促进宫颈癌细胞自噬和凋亡。
引用本文:石艳,刘明,黄艳,张军,尹玲,“rxra调控PLD1对长链非编码RNA LINC00511的抑制促进宫颈癌细胞自噬和凋亡的作用”,《细胞生理杂志》,第35期,no。10(2020): 6592-6604。https://doi.org/10.1002/jcp.29529。上述文章于2020年2月17日在线发表在Wiley在线图书馆(wileyonlinelibrary.com)上,经期刊主编Robert Heath同意撤回;和Wiley期刊有限责任公司。第三方报告说,在这篇文章中,图像共享了图5D中重叠的部分,并且这种复制得到了出版商的证实。第三方还报告,图5a中使用的肿瘤测量尺与不同作者先前发表的文章中使用的尺相同,每一篇文章都描述了不同的科学背景(Chen, et al. 2019 [https://doi.org/10.1002/jcp.28911]]和(Feng, et al. 2019 [https://doi.org/10.1186/s13287-022-02841-z]])。在来自不同机构的不相关研究小组的不同文章的数字中使用相同的尺子,这使所报告数据的准确性受到怀疑。作者没有回应出版商的询问。由于本文中图像重复的证据,以及不同作者无法解释的图像元素和设备与其他实验的重复,从根本上损害了本文报告的结论,因此同意撤回。作者没有回应我们关于撤稿的通知。
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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