Skip to main content
Frontiers in Immunology logoLink to Frontiers in Immunology
. 2026 Mar 13;17:1820769. doi: 10.3389/fimmu.2026.1820769

Correction: RARS1 inhibits ENO1 ubiquitination and degradation to protect against ferroptosis in hepatocellular carcinoma

Shouge Zang 1, Jvlong Ma 1, Lichang Chen 2, Di Cui 3,*,†, Jiangtao Yu 1,*,†
PMCID: PMC13022709  PMID: 41909659

There was a mistake in Figure 9B as published: the β-Actin band was incorrectly used during figure preparation. The corrected Figure 9B appears below:

Figure 9.

Panel A contains a scatter plot highlighting AH.6809 among other compounds and a structural diagram of AH.6809. Panel B displays a western blot for β-Actin and RARS1 with increasing concentrations of AH.6809. Panel C shows two line graphs depicting rising OD values over time for Huh7 and SKHep1 cells, both with and without AH.6809. Panel D provides colony formation assay images for Huh7 and SKHep1 cells treated with either NC or AH.6809, with a bar chart quantifying colony number. Panel E shows wound-healing assays at zero and twenty-four hours for both cell lines, along with a bar graph of relative gap distances. Panel F presents migration assay images for each group with an adjacent bar graph showing quantified cell numbers.

AH-6809 inhibits RARS1 expression and suppresses LIHC cell proliferation, migration, and invasion. (A) Connectivity Map (cMAP) analysis identifying potential small-molecule inhibitors targeting RARS1. AH-6809 showed a strong negative correlation with the RARS1 gene expression signature and was selected for further validation. (B) Western blot analysis of RARS1 protein levels in Huh7 cells treated with increasing concentrations of AH-6809 (0, 10, 20, and 40 nmol). RARS1 expression decreased in a dose-dependent manner. (C) Cell proliferation assessed by CCK-8 assay in Huh7 and SKHep1 cells treated with 20 nmol AH-6809 for 24–96 (h) AH-6809 significantly reduced cell viability compared with the control group. (D) Colony formation assay showing that AH-6809 markedly decreased the number and size of colonies in Huh7 and SKHep1 cells. (E) Wound-healing assay showing inhibition of cell migration after 24 h of AH-6809 treatment. (F) Transwell invasion assay showing that AH-6809 significantly reduced the number of invasive cells in both Huh7 and SKHep1 lines. All cell-based assays (CCK-8, colony formation, wound-healing, Transwell, and Western blot) were conducted in triplicate (n = 3). Data were shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001.

There was a mistake in the caption of Supplementary Figure 3 as published. During the second round of review and revision, the authors forgot to remove the caption for Supplementary Figure 3D. The corrected caption of Supplementary Figure 3 appears below:

Drug sensitivity analysis and potential small molecule targeting RARS1. (A) Drug sensitivity analysis conducted using the GSCA database revealed a strong association between RARS1 expression and resistance to various chemotherapy agents. The correlation between RARS1 and drug sensitivity is visualized through a correlation matrix showing the relationship between gene expression and chemotherapy efficacy. (B) Molecular docking analysis of AH.6809 binding to RARS1 revealed multiple binding sites, including hydrogen bonding and hydrophobic interactions. The 3D structure of RARS1 is shown with AH.6809 binding in the active site, and the detailed molecular interactions between AH.6809 and RARS1 are illustrated.

The original version of this article has been updated.

Footnotes

Edited and reviewed by: Praveen Koganti, Sanford Burnham Prebys Medical Discovery Institute, United States

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.


Articles from Frontiers in Immunology are provided here courtesy of Frontiers Media SA

RESOURCES