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Corrigendum Open Access | 10.1172/JCI171901

RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse

Jaebeom Cho, Hye-Young Min, Ho Jin Lee, Seung Yeob Hyun, Jeong Yeon Sim, Myungkyung Noh, Su Jung Hwang, Shin-Hyung Park, Hye-Jin Boo, Hyo-Jong Lee, Sungyoul Hong, Rang-Woon Park, Young Kee Shin, Mien-Chie Hung, and Ho-Young Lee

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Published May 15, 2023 - More info

Published in Volume 133, Issue 10 on May 15, 2023
J Clin Invest. 2023;133(10):e171901. https://doi.org/10.1172/JCI171901.
© 2023 Cho 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 May 15, 2023 - Version history
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Related article:

RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse
Jaebeom Cho, … , Mien-Chie Hung, Ho-Young Lee
Jaebeom Cho, … , Mien-Chie Hung, Ho-Young Lee
Research Article Cell biology Oncology

RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse

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Abstract

Slow-cycling/dormant cancer cells (SCCs) have pivotal roles in driving cancer relapse and drug resistance. A mechanistic explanation for cancer cell dormancy and therapeutic strategies targeting SCCs are necessary to improve patient prognosis, but are limited because of technical challenges to obtaining SCCs. Here, by applying proliferation-sensitive dyes and chemotherapeutics to non–small cell lung cancer (NSCLC) cell lines and patient-derived xenografts, we identified a distinct SCC subpopulation that resembled SCCs in patient tumors. These SCCs displayed major dormancy-like phenotypes and high survival capacity under hostile microenvironments through transcriptional upregulation of regulator of G protein signaling 2 (RGS2). Database analysis revealed RGS2 as a biomarker of retarded proliferation and poor prognosis in NSCLC. We showed that RGS2 caused prolonged translational arrest in SCCs through persistent eukaryotic initiation factor 2 (eIF2α) phosphorylation via proteasome-mediated degradation of activating transcription factor 4 (ATF4). Translational activation through RGS2 antagonism or the use of phosphodiesterase 5 inhibitors, including sildenafil (Viagra), promoted ER stress–induced apoptosis in SCCs in vitro and in vivo under stressed conditions, such as those induced by chemotherapy. Our results suggest that a low-dose chemotherapy and translation-instigating pharmacological intervention in combination is an effective strategy to prevent tumor progression in NSCLC patients after rigorous chemotherapy.

Authors

Jaebeom Cho, Hye-Young Min, Ho Jin Lee, Seung Yeob Hyun, Jeong Yeon Sim, Myungkyung Noh, Su Jung Hwang, Shin-Hyung Park, Hye-Jin Boo, Hyo-Jong Lee, Sungyoul Hong, Rang-Woon Park, Young Kee Shin, Mien-Chie Hung, Ho-Young Lee

×

Original citation: J Clin Invest. 2021;131(1):e136779. https://doi.org/10.1172/JCI136779

Citation for this corrigendum: J Clin Invest. 2023;133(10):e171901. https://doi.org/10.1172/JCI171901

The authors recently became aware of an inadvertent error in Figure 3E. In the original version of Figure 3E, the H1299 Cyclin D1 blot was incorrect and was the same as the SK Cyclin D1 blot. The correct figure is shown below. The HTML and PDF versions have been updated online.

The authors regret the error.

Footnotes

See the related article at RGS2-mediated translational control mediates cancer cell dormancy and tumor relapse.

Version history
  • Version 1 (May 15, 2023): Electronic publication

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