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CORRECTION article

Front. Oncol., 13 January 2026

Sec. Gynecological Oncology

Volume 16 - 2026 | https://doi.org/10.3389/fonc.2026.1765010

Correction: PRKCI mediates radiosensitivity via the Hedgehog/GLI1 pathway in cervical cancer

This article is a correction to:

  1. PRKCI Mediates Radiosensitivity via the Hedgehog/GLI1 Pathway in Cervical Cancer

    1. Read original article
Zhuna Wu,,&#x;Zhuna Wu1,2,3†Chunxian Huang,&#x;Chunxian Huang1,2†Ruixin Li,Ruixin Li1,2Hui Li,Hui Li1,2Huaiwu Lu,*Huaiwu Lu1,2*Zhongqiu Lin,*Zhongqiu Lin1,2*
  • 1Department of Gynecological Oncology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China
  • 2Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
  • 3Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Fujian Medical University, Fujian Medical University, Quanzhou, China

A Correction on
PRKCI mediates radiosensitivity via the Hedgehog/GLI1 pathway in cervical cancer

By Wu Z, Huang C, Li R, Li H, Lu H and Lin Z (2022) Front. Oncol. 12:887139. doi: 10.3389/fonc.2022.887139

There was a mistake in Figure 7C as published. The panels representing SiHa cells treated with Auranofin at 6 Gy and 8 Gy radiation doses were inadvertently duplicated during the figure assembly process. This duplication was unintentional and does not reflect the underlying experimental data, which remain valid and consistent with the original findings. The corrected Figure 7C appears below. The panels for 6 Gy and 8 Gy Auranofin treatment in SiHa cells are distinct and accurately represent the original exp erimental results. No other text, data, figures, or conclusions in the manuscript are affected by this change.

Figure 7
A multi-panel scientific illustration depicts the effects of Auranofin on Hela and Siha cells. Panel A shows a schematic of Auranofin inducing cell death and tumor inhibition via PKCI pathway. Panel B presents a dose-response curve of cell viability in Hela and Siha cells treated with Auranofin. Panel C displays colony formation assays under different irradiation doses with survival fractions graphed. Panel D includes bar charts of cell proliferation over time. Panel E shows flow cytometry analyses of cell cycle phases. Panel F illustrates apoptotic cell percentages via Annexin V APC-A assay. Panel G includes images of tumor samples with corresponding weight and size measurements graphed in Panel H. Panel I shows mouse body weight charts. Panel J summarizes the molecular mechanism of Auranofin action, emphasizing inhibition of proliferation, increased apoptosis, and cell cycle arrest.

Figure 7. AF, a selective inhibitor of PKCI, affected radiosensitivity in CC cells in vitro and in vivo. (A) Workflow for AF-mediated radiosensitivity of CC in vitro and in vivo. (B) Representative IC50 curves calculated for AF in HeLa and SiHa cells are shown. (C) In colony formation assays, AF affected the proliferation of HeLa and SiHa cells treated with radiotherapy in a dose-dependent manner. (D) The cell viability of AF-treated HeLa and SiHa cells after radiotherapy at 8 Gy by CCK-8 assays. (E) AF-induced G2/M-phase cell cycle arrest with radiotherapy. (F) AF increased apoptosis of HeLa and SiHa cells treated with radiotherapy. (G) Nude mouse models were treated by intraperitoneal injection with AF or 0.1% DMSO before irradiation. (H) The xenograft weights and volumes were measured (n = 5/group). (I) Mice from two groups (AF group and control group, 5 mice per group) were weighed during the course of treatments. (J) A cartoon model indicating the role of PRKCI as an oncogene regulates radiosensitivity by modulating GLI1 relocalization and phosphorylation in CC via the Hh/GLI1 pathway. Data are shown as the mean from three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001 by multiple t-tests (C, D, G, I), by unpaired t-tests (E, F, H) ns,not significant. AF, auranofin; CC, cervical cancer; IC50, half-maximal inhibitory concentration; CCK-8, Cell Counting Kit-8; DMSO, dimethyl sulfoxide. ns, not significant.

The original version of this article has been updated.

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.

Keywords: PRKCI, radiosensitivity, Hedgehog/GLI1 pathway, cervical cancer, auranofin

Citation: Wu Z, Huang C, Li R, Li H, Lu H and Lin Z (2026) Correction: PRKCI mediates radiosensitivity via the Hedgehog/GLI1 pathway in cervical cancer. Front. Oncol. 16:1765010. doi: 10.3389/fonc.2026.1765010

Received: 10 December 2025; Accepted: 06 January 2026;
Published: 13 January 2026.

Edited and reviewed by:

Carlos Gil Ferreira, Instituto Oncoclínicas, Brazil

Copyright © 2026 Wu, Huang, Li, Li, Lu and Lin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Huaiwu Lu, bHVodWFpd3VAbWFpbC5zeXN1LmVkdS5jbg==; Zhongqiu Lin, bGluLXpob25ncWl1QDE2My5jb20=

†These authors have contributed equally to this work

Disclaimer: 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.