RETRACTION: Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma

IF 3 3区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of cellular biochemistry Pub Date : 2024-09-30 DOI:10.1002/jcb.30650

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Abstract

RETRACTION: Z. Zhao, T. Liang, and S. Feng, “Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma,” Journal of Cellular Biochemistry 120, no. 7 (2019): 11510-11516, https://doi.org/10.1002/jcb.28430.

The above article, published online on 20 February 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, image elements in Figure 4 were found to have been previously published in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. The authors have been informed of the decision of retraction but unavailable for a final confirmation.

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回归：抑制 HAS2-AS1 通过 PI3K/AKT 信号通路抑制胶质瘤的细胞增殖、迁移和侵袭。

撤回：Z. Zhao, T. Liang, and S. Feng, "Silencing of HAS2-AS1 Mediates PI3K/AKT Signaling Pathway to Inhibit Cell Proliferation, Migration, and Invasion in Glioma," Journal of Cellular Biochemistry 120, no：11510-11516, https://doi.org/10.1002/jcb.28430.The 上述文章于 2019 年 2 月 20 日在线发表于 Wiley Online Library (wileyonlinelibrary.com)，经期刊主编 Christian Behl 和 Wiley Periodicals LLC 协议，已被撤回。同意撤稿的原因是第三方对文章中提供的数据提出了疑虑。我们发现文章中介绍的结果与实验方法之间存在若干缺陷和不一致之处。此外，还发现图 4 中的图像元素以前曾在不同的科学背景下发表过。因此，编辑认为这篇文章的结论无效。作者已被告知撤稿决定，但尚未得到最终确认。

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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来源期刊

Journal of cellular biochemistry 生物-生化与分子生物学

CiteScore

9.90

自引率

0.00%

发文量

164

审稿时长

1 months

期刊介绍： The Journal of Cellular Biochemistry publishes descriptions of original research in which complex cellular, pathogenic, clinical, or animal model systems are studied by biochemical, molecular, genetic, epigenetic or quantitative ultrastructural approaches. Submission of papers reporting genomic, proteomic, bioinformatics and systems biology approaches to identify and characterize parameters of biological control in a cellular context are encouraged. The areas covered include, but are not restricted to, conditions, agents, regulatory networks, or differentiation states that influence structure, cell cycle & growth control, structure-function relationships.