撤稿:"H19通过miR-675/FADD和miR-138/PTK2信号通路促进肝母细胞瘤细胞凋亡,从而抑制其生长

IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
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引用次数: 0

摘要

撤稿:"H19通过miR-675/FADD和miR-138/PTK2的信号通路促进肝母细胞瘤细胞凋亡从而抑制其生长",作者:葛丽丽、张先伟、胡胜男、宋银森、孔景辉、张博、杨晓刚,J Cell Biochem 2019, 120: 5218-5231。上述文章于2018年10月26日在线发表于《Wiley Online Library》(https://doi.org/10.1002/jcb.27797),经作者、该杂志主编Christian Behl和Wiley Periodicals LLC三方协商,决定撤回该文章。在作者提出撤回请求后,决定撤回该文章。初步评估发现图 2A 和图 2C 的图像元素存在重复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Retraction: “H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR-675/FADD and miR-138/PTK2”

Retraction: “H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR-675/FADD and miR-138/PTK2” by Lili Ge, Xianwei Zhang, Shengnan Hu, Yinsen Song, Jinghui Kong, Bo Zhang, Xiaoang Yang, J Cell Biochem 2019, 120: 5218-5231. The above article, published online on 26 October 2018 in Wiley Online Library (https://doi.org/10.1002/jcb.27797) has been retracted by agreement between the authors, the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The decision to retract the article was made following a request for retraction from the authors. An initial assessment uncovered the duplication of image elements between Figure 2A and 2C.

The editors believe that these findings compromise the interpretation of the data and results presented.

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来源期刊
Journal of cellular biochemistry
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.
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