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Corrigendum Open Access | 10.1172/JCI200436

Corrigendum to The polycomb group protein Bmi-1 represses the tumor suppressor PTEN and induces epithelial-mesenchymal transition in human nasopharyngeal epithelial cells

Li-Bing Song, Jun Li, Wen-Ting Liao, Yan Feng, Chun-Ping Yu, Li-Juan Hu, Qing-Li Kong, Li-Hua Xu, Xing Zhang, Wan-Li Liu, Man-Zhi Li, Ling Zhang, Tie-Bang Kang, Li-Wu Fu, Wen-Lin Huang, Yun-Fei Xia, Sai Wah Tsao, Mengfeng Li, Vimla Band, Hamid Band, Qing-Hua Shi, Yi-Xin Zeng, and Mu-Sheng Zeng

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Published November 3, 2025 - More info

Published in Volume 135, Issue 21 on November 3, 2025
J Clin Invest. 2025;135(21):e200436. https://doi.org/10.1172/JCI200436.
© 2025 Song et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published November 3, 2025 - Version history
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The polycomb group protein Bmi-1 represses the tumor suppressor PTEN and induces epithelial-mesenchymal transition in human nasopharyngeal epithelial cells
Li-Bing Song, … , Yi-Xin Zeng, Mu-Sheng Zeng
Li-Bing Song, … , Yi-Xin Zeng, Mu-Sheng Zeng
Research Article Oncology

The polycomb group protein Bmi-1 represses the tumor suppressor PTEN and induces epithelial-mesenchymal transition in human nasopharyngeal epithelial cells

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Abstract

The polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) is dysregulated in various cancers, and its upregulation strongly correlates with an invasive phenotype and poor prognosis in patients with nasopharyngeal carcinomas. However, the underlying mechanism of Bmi-1–mediated invasiveness remains unknown. In the current study, we found that upregulation of Bmi-1 induced epithelial-mesenchymal transition (EMT) and enhanced the motility and invasiveness of human nasopharyngeal epithelial cells, whereas silencing endogenous Bmi-1 expression reversed EMT and reduced motility. Furthermore, upregulation of Bmi-1 led to the stabilization of Snail, a transcriptional repressor associated with EMT, via modulation of PI3K/Akt/GSK-3β signaling. Chromatin immunoprecipitation assays revealed that Bmi-1 transcriptionally downregulated expression of the tumor suppressor PTEN in tumor cells through direct association with the PTEN locus. This in vitro analysis was consistent with the statistical inverse correlation detected between Bmi-1 and PTEN expression in a cohort of human nasopharyngeal carcinoma biopsies. Moreover, ablation of PTEN expression partially rescued the migratory/invasive phenotype of Bmi-1–silenced cells, indicating that PTEN might be a major mediator of Bmi-1–induced EMT. Our results provide functional and mechanistic links between the oncoprotein Bmi-1 and the tumor suppressor PTEN in the development and progression of cancer.

Authors

Li-Bing Song, Jun Li, Wen-Ting Liao, Yan Feng, Chun-Ping Yu, Li-Juan Hu, Qing-Li Kong, Li-Hua Xu, Xing Zhang, Wan-Li Liu, Man-Zhi Li, Ling Zhang, Tie-Bang Kang, Li-Wu Fu, Wen-Lin Huang, Yun-Fei Xia, Sai Wah Tsao, Mengfeng Li, Vimla Band, Hamid Band, Qing-Hua Shi, Yi-Xin Zeng, Mu-Sheng Zeng

×

Original citation: J Clin Invest. 2009;119(12):3626–3636. https://doi.org/10.1172/JCI39374

Citation for this corrigendum: J Clin Invest. 2025;135(21):e200436. https://doi.org/10.1172/JCI200436

The authors became aware that in Figure 3A, the GSK3β blot for the NPEC2 cells was inadvertently duplicated in the CNE2 panel. In addition, in Supplemental Figure 6A, the representative image for 24-hour Bmi1 shRNA#2 + PTEN shRNA#2 (row 3, column 4) was inadvertently duplicated from the representative image for 24-hour Bmi1 shRNA#2 + PTEN shRNA#1 (row 3, column 3). The correct Figure 3A is shown below and an updated version of the supplemental material has been provided.

Figure 3A

The authors regret the errors.

Supplemental material

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Footnotes

See the related article at The polycomb group protein Bmi-1 represses the tumor suppressor PTEN and induces epithelial-mesenchymal transition in human nasopharyngeal epithelial cells.

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