Correction to: “O-GlcNAcylation promotes the migratory ability of hepatocellular carcinoma cells via regulating FOXA2 stability and transcriptional activity”

IF 4.5 2区生物学 Q2 CELL BIOLOGY Journal of Cellular Physiology Pub Date : 2024-07-18 DOI:10.1002/jcp.31381

引用次数: 0

Abstract

Huang, H., Wu, Q., Guo, X., Huang, T., Xie, X., Wang, L., Liu, Y., Shi, L., Li, W., Zhang, J., & Liu, Y. (2021). O-GlcNAcylation promotes the migratory ability of hepatocellular carcinoma cells via regulating FOXA2 stability and transcriptional activity. J Cell Physiol, 236, 7491–7503. https://doi.org/10.1002/jcp.30385

In the first published version of this manuscript, a transwell migration microscope image presented in Figure 6b of the HepG2 Mock group was accidentally misused during the assembly of the figures, resulting in image duplication. In the corrected Figure 6b below, the photo corresponding to HepG2 Mock group has been replaced with the original and accurate one.

The authors regret the initial mistake in manuscript preparation. This error does not affect the scientific validity of the conclusions of this study. The authors apologize for any confusion they may have caused.

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更正："O-GlcNAcylation通过调节FOXA2的稳定性和转录活性促进肝癌细胞的迁移能力"。

Huang, H., Wu, Q., Guo, X., Huang, T., Xie, X., Wang, L., Liu, Y., Shi, L., Li, W., Zhang, J., & Liu, Y. (2021)。O-GlcNAcylation 通过调控 FOXA2 的稳定性和转录活性促进肝癌细胞的迁移能力。J Cell Physiol, 236, 7491-7503. https://doi.org/10.1002/jcp.30385In 在本稿件首次发表的版本中，HepG2 Mock 组图 6b 中的一张 transwell 迁移显微镜图像在组装图时被意外误用，导致图像重复。在以下更正后的图 6b 中，与 HepG2 Mock 组对应的照片已替换为准确的原始照片。这一错误并不影响本研究结论的科学性。对于可能造成的混淆，作者深表歉意。

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 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.