Front. Oncol. Frontiers in Oncology Front. Oncol. 2234-943X Frontiers Media S.A. 10.3389/fonc.2025.1637363 Oncology Correction Correction: FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway Li Yiming 1 2 † Liang Jianshen 1 2 3 † Ren Xiude 1 2 † Guo Jiahe 1 2 3 Wang Xisen 1 2 3 Wang Xuya 1 2 3 Yu Shengping 1 2 Li Tao 1 2 * Yang Xuejun 1 2 3 * 1 Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China 2 Laboratory of Neuro-Oncology, Tianjin Medical University General Hospital, Tianjin, China 3 Department of Neurosurgery, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua Medicine, Tsinghua University, Beijing, China

Edited and Reviewed by: Dan Liu, Sichuan University, China

*Correspondence: Xuejun Yang, ydenny@126.com; Tao Li, litao@tmu.edu.cn

†These authors have contributed equally to this work

 02 07 2025 2025 15 1637363 30 05 2025 04 06 2025 Copyright © 2025 Li, Liang, Ren, Guo, Wang, Wang, Yu, Li and Yang 2025 Li, Liang, Ren, Guo, Wang, Wang, Yu, Li and Yang

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 A Correction on FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway by Li Y, Liang J, Ren X, Guo J, Wang X, Wang X, Yu S, Li T and Yang X (2025). Front. Oncol. 15:1560008. doi: 10.3389/fonc.2025.1560008 FGFR3-TACC3 fusion gene glioma malignant progression invasion migration STAT3 signaling pathway section-in-acceptance Cancer Molecular Targets and Therapeutics

In the published article, there was an error in Figure 1F and Figure 3J as published. The error in the image presented in Figure 1F (U87MG F3-T3 K508R and U87MG Empty vector) and an incorrect use of scale bar in Figure 3J . The corrected Figure 1 , Figure 3 and their captions appear below.

F3-T3 significantly promoted the proliferation, invasion, and migration of glioma cells. (A) Correlation of FGFR3 expression with prognosis in glioma patients from the TCGA database: The Kaplan-Meier plotter showed Glioma patients with higher FGFR3 expression reached poorer prognosis than those expressed lower. (B) GSEA results of F3-T3 and empty vector based on the GSE42401 database. The GSEA results showed F3-T3 glioma cells enriched in several key signaling pathways that closely correlated with cancer. (C) Western blot analysis showing expression levels of p-FGFR and FGFR3 in cells transfected with F3-T3, F3-T3 K508R, and empty vector. (D) CCK-8 assay results indicating enhanced proliferation of U87MG and U251MG cells expressing F3-T3 compared to those with F3-T3 K508R mutant and empty vector. (E) EdU labeling assay demonstrating increased proliferation in U87MG and U251MG cells due to F3-T3 expression. (F) Colony formation assay results showing higher colony formation efficiency in glioma cells expressing F3-T3 compared to control groups. (G) Wound healing assay results revealing increased invasion capability in glioma cells with F3-T3 expression compared to cells with F3-T3 K508R mutant and empty vector. (H) Transwell assays for invasion and migration showing that F3-T3 can significantly enhance these abilities in glioma cells compared to F3-T3 K508R and empty vector. (***p<0.001, ****p<0.00001)..

A composite image presents various scientific data panels related to FGFR3 expression in U251MG and U87MG cell lines. Panel A shows a survival probability graph comparing low and high FGFR3 expression groups. Panel B consists of three line graphs displaying gene set enrichment analysis results for actin filament movement, cell migration, and epithelial-mesenchymal transition. Panel C displays Western blot results for FGFR3 and related proteins. Panel D presents growth curves for different treatments. Panel E illustrates fluorescent microscopy images showing DAPI, EdU, and merged staining. Panel F shows colony formation assays. Panel G depicts wound healing assays at different time intervals. Panel H displays images from invasion and migration assays.

STAT3 was closely associated with the WHO grade, IDH wild-type status, 1p/19q chromosome co-deletion and worse prognosis, as well as being closely linked to EMT. (A) Expression profile of STAT3 across 33 different cancer types and their corresponding normal tissues, as shown in the TCGA database. Our analysis revealed that in 9 of the 33 malignant tumor types, the expression profiles did not match those of their corresponding normal tissues, these malignant tumors including lymphoid neoplasm diffuse large B-cell lymphoma (DLBC), adrenocortical carcinoma (AAC), brain lower grade glioma (LGG), mesothelioma (MESO), acute myeloid leukemia (LAML), uveal melanoma (UVM), testicular germ cell tumors (TCGT), ovarian serous cystadenocarcinoma (OV), and uterine carcinosarcoma (UCS). Among the remaining 24 cancer types, 12 exhibited statistically significant differences in STAT3 expression levels between tumor and normal tissues. These cancers included bladder and urothelial carcinoma (BLCA), esophageal carcinoma (ESCA), cholangiocarcinoma (CHOL), glioblastoma (GBM), kidney renal clear cell carcinoma (KIRC), head and neck squamous cell carcinoma (HNSC), kidney chromophobe (KICH), lung adenocarcinoma (LUAD), kidney renal papillary cell carcinoma (KIRP), stomach adenocarcinoma (STAD), lung squamous cell carcinoma (LUSC), and prostate adenocarcinoma (PRAD). In contrast, the other 12 cancers did not show statistically significant differences. Specifically, five cancer types demonstrated elevated STAT3 expression in tumor tissues, including cholangiocarcinoma (CHOL), glioblastoma (GBM), esophageal carcinoma (ESCA), head and neck squamous cell carcinoma (HNSC), and stomach adenocarcinoma (STAD), while seven showed higher expression in normal tissues, including bladder and urothelial carcinoma (BLCA), kidney renal clear cell carcinoma (KIRC), kidney chromophobe (KICH), lung squamous cell carcinoma (LUSC), kidney renal papillary cell carcinoma (KIRP), lung adenocarcinoma (LUAD), and prostate adenocarcinoma (PRAD). Notably, GBM exhibited a marked difference in STAT3 expression between tumor and normal tissues (p < 0.001). (B–D) Kaplan-Meier survival curves analyzing the overall survival, progression-free interval, and disease-specific survival of glioma patients categorized by high versus low STAT3 expression. The curves indicate that higher STAT3 expression was associated with poorer prognosis in glioma patients. (E–G) Correlation analysis between STAT3 expression levels and clinical parameters in glioma, including WHO grades, 1p/19q chromosome co-deletion status, and IDH mutation status, utilizing the TCGA database. The analysis results shows that STAT3 expression was significantly linked to these clinical indicators. (H) GSEA analysis revealed a strong correlation between STAT3 expression and the EMT process, with a NES of 2.1825 and an adjusted p-value < 0.001. (I, J) Analysis of p-STAT3 expression in GBM, demonstrating significantly higher levels compared to lower-grade gliomas. (K) Enlarged histological image results of (J). (*p<0.05, **p<0.01, ***p<0.001, ****p<0.00001).

A series of data visualizations analyzing STAT3 expression in tumors. Panel A shows box plots comparing STAT3 expression in various cancer types. Panel B displays an overall survival curve related to STAT3. Panels C and D present progression-free and disease-specific survival curves. Panels E, F, and G show box plots of STAT3 expression across WHO grades and IDH status. Panel H features a graph of epithelial-mesenchymal transition enrichment. Panel I is a bar chart of p-STAT3 protein expression in gliomas. Panels J and K depict histological images of tumors with different WHO grades, showing variations in staining.

The original version of this article has been updated.

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