Following the publication of this article [1], concerns were raised regarding results presented in Fig 1. Specifically,
- The Fig 1A OPM-2 actin panel and the Fig 1C PT#4 actin panel appear similar when horizontally stretched despite representing different experimental conditions.
- Lanes 2–4 of the Fig 1A ANBL6/U266/8226 actin panel appear similar to the Fig 3A shRNA MNK2 GAPDH panel.
- The Fig 1C PT#2 P-MNK and T-MNK panels of [1] appear similar to the Figure 1B OPM-2 FKHD-P and FKHD-T panels of [2] respectively.
- In Fig 1D, the MNK1 panel in the MNK2 immunoprecipitation blot has no detectable signal nor does the panel present a positive control to confirm a successful blot.
The authors did not provide the raw data underlying the published results for editorial review. In the absence of the raw data required to support the published results PLOS is unable to resolve the above issues.
In light of the concerns affecting multiple figure panels that question the validity and reliability of these data, the PLOS ONE Editors retract this article.
CB and JG agreed with the retraction. PF did not agree with the retraction. YS, BH, YY, and AL either did not respond directly or could not be reached.
References
- 1. Shi Y, Frost P, Hoang B, Yang Y, Bardeleben C, Gera J, et al. (2014) MNK1-Induced eIF-4E Phosphorylation in Myeloma Cells: A Pathway Mediating IL-6-Induced Expansion and Expression of Genes Involved in Metabolic and Proteotoxic Responses. PLoS ONE 9(4): e94011. pmid:24714040
- 2. Shi Y, Yan H, Frost P, Gera J & Lichtenstein A. (2005) Mammalian target of rapamycin inhibitors activate the AKT kinase in multiple myeloma cells by up-regulating the insulin-like growth factor receptor/insulin receptor substrate-1/phosphatidylinositol 3-kinase cascade. Mol Cancer Ther 4(10): 1533–1540. pmid:16227402
Citation: The PLOS ONE Editors (2023) Retraction: MNK1-Induced eIF-4E Phosphorylation in Myeloma Cells: A Pathway Mediating IL-6-Induced Expansion and Expression of Genes Involved in Metabolic and Proteotoxic Responses. PLoS ONE 18(9): e0291491. https://doi.org/10.1371/journal.pone.0291491
Published: September 8, 2023
Copyright: © 2023 The PLOS ONE Editors. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.