RETRACTION

Pathol. Oncol. Res., 25 May 2023

Volume 29 - 2023 | https://doi.org/10.3389/pore.2023.1611110

Retraction: MiR-543 Inhibits the Migration and Epithelial-To-Mesenchymal Transition of TGF-β-Treated Endometrial Stromal Cells via the MAPK and Wnt/β-Catenin Signaling Pathways

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Following publication, concerns were raised regarding data misrepresentation. In particular, with the Western blot in Figure 4A, which also appears in Zhang et al. [1]. Following provision of raw data by the authors, the Editor in Chief concluded that the article’s conclusions and assertions were not sufficiently supported by the findings from the material provided; therefore, the article has been retracted.

References

  • 1

    Zhang M Liu S Fang L Wang G Yin L . Asiaticoside inhibits renal fibrosis development by regulating the miR-142-5p/ACTN4 axis. Biotechnol Appl Biochem (2022) 69:31322. 10.1002/bab.2110

Summary

Keywords

molecular biology, miRNA-543, MAPK, Wnt/B-catenin, endometrial stromal cell

Citation

Pathology and Oncology Research Editorial Office (2023) Retraction: MiR-543 Inhibits the Migration and Epithelial-To-Mesenchymal Transition of TGF-β-Treated Endometrial Stromal Cells via the MAPK and Wnt/β-Catenin Signaling Pathways. Pathol. Oncol. Res. 29:1611110. doi: 10.3389/pore.2023.1611110

Received

10 February 2023

Accepted

10 February 2023

Published

25 May 2023

Approved by

Pathology & Oncology Research Editorial Office

Volume

29 - 2023

Updates

Copyright

© 2023 Pathology and Oncology Research Editorial Office.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Pathology and Oncology Research Editorial Office,

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