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Corrigendum Free access | 10.1172/JCI155916

MicroRNA-30e* promotes human glioma cell invasiveness in an orthotopic xenotransplantation model by disrupting the NF-κB/IκBα negative feedback loop

Lili Jiang, Chuyong Lin, Libing Song, Jueheng Wu, Baixue Chen, Zhe Ying, Lishan Fang, Xiao Yan, Mian He, Jun Li, and Mengfeng Li

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Published November 15, 2021 - More info

Published in Volume 131, Issue 22 on November 15, 2021
J Clin Invest. 2021;131(22):e155916. https://doi.org/10.1172/JCI155916.
© 2021 American Society for Clinical Investigation
Published November 15, 2021 - Version history
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MicroRNA-30e* promotes human glioma cell invasiveness in an orthotopic xenotransplantation model by disrupting the NF-κB/IκBα negative feedback loop
Lili Jiang, … , Jun Li, Mengfeng Li
Lili Jiang, … , Jun Li, Mengfeng Li
Research Article

MicroRNA-30e* promotes human glioma cell invasiveness in an orthotopic xenotransplantation model by disrupting the NF-κB/IκBα negative feedback loop

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Abstract

Constitutive activation of NF-κB is a frequent event in human cancers, playing important roles in cancer development and progression. In nontransformed cells, NF-κB activation is tightly controlled by IκBs. IκBs bind NF-κB in the cytoplasm, preventing it from translocating to the nucleus to modulate gene expression. Stimuli that activate NF-κB signaling trigger IκB degradation, enabling nuclear translocation of NF-κB. Among the genes regulated by NF-κB are those encoding the IκBs, providing a negative feedback loop that limits NF-κB activity. How transformed cells override this NF-κB/IκB negative feedback loop remains unclear. Here, we report in human glioma cell lines that microRNA-30e* (miR-30e*) directly targets the IκBα 3ι-UTR and suppresses IκBα expression. Overexpression of miR-30e* in human glioma cell lines led to hyperactivation of NF-κB and enhanced expression of NF-κB–regulated genes, which promoted glioma cell invasiveness in in vitro assays and in an orthotopic xenotransplantation model. These effects of miR-30e* were shown to be clinically relevant, as miR-30e* was found to be upregulated in primary human glioma cells and correlated with malignant progression and poor survival. Hence, miR-30e* provides an epigenetic mechanism that disrupts the NF-κB/IκBα loop and may represent a new therapeutic target and prognostic marker.

Authors

Lili Jiang, Chuyong Lin, Libing Song, Jueheng Wu, Baixue Chen, Zhe Ying, Lishan Fang, Xiao Yan, Mian He, Jun Li, Mengfeng Li

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Original citation: J Clin Invest. 2012;122(1):33–47. https://doi.org/10.1172/JCI58849

Citation for this corrigendum: J Clin Invest. 2021;131(22):e155916.. https://doi.org/10.1172/JCI155916

The authors recently became aware that the image presented in the original Supplemental Figure 5D as miR-30e* PGC#2 was identical to the image in Supplemental Figure 8E, NC U87MG-miR-30e/30e*, and that the image presented in the original Supplemental Figure 5E as miR-30e* inhibitor PGC#2 was identical to the image in Figure 8A, miR-30e* inhibitor U87MG. After review of the original data, the authors determined that the errors were made in Supplemental Figure 5E and Supplemental Figure 5D. An institutional review committee concluded that the errors in Supplemental Figure 5D and Supplemental Figure 5E were inadvertent and recommended correction. The authors provided the correct version of Supplemental Figure 5D and Supplemental Figure 5E with data obtained from repeated experiments. The correct version is shown below and in the updated supplemental data.

Supplemental Figure 5

The authors regret the errors.

Footnotes

See the related article at MicroRNA-30e* promotes human glioma cell invasiveness in an orthotopic xenotransplantation model by disrupting the NF-κB/IκBα negative feedback loop.

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  • Version 1 (November 15, 2021): Electronic publication

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