Authors
Bing Liao, Liwei Zhang, Qiuren Zou, Meiqun Wang, Jianguo Liu, Liqing Guo, Zhichao Zhou, Yun Yi
Published in
Molecular and cellular probes. Pages 102092. Oct 31, 2026. Epub Oct 31, 2026.
Abstract
Radiotherapy resistance is a major cause of treatment failure in nasopharyngeal carcinoma (NPC). Elucidating the mechanisms underlying NPC radiotherapy resistance holds great importance for optimizing NPC treatment strategies. In this study, a radiotherapy-resistant NPC cell model (CNE-2R) was established using graded ionizing radiation (IR). Abnormally high expression levels of YTHDF1 and SATB1 were observed in NPC cells, particularly in CNE-2R. Subsequently, we constructed CNE-2R cells with YTHDF1 knockdown (siYTHDF1) and evaluated the impact of YTHDF1 knockdown on the biological functions of CNE-2R cells through EdU assay, Transwell assay, ELISA, and flow cytometry. The results demonstrated that knockdown of YTHDF1 inhibited the proliferation, invasion, and migration abilities of CNE-2R cells, and induced cell apoptosis. Pearson correlation analysis revealed a positive correlation between YTHDF1 and SATB1 expression. Meanwhile, Western blot results indicated that knockdown of YTHDF1 reduced the expression of SATB1, Wnt1, β-catenin, and cyclin D1. Further investigation using m6A-IP and CLIP assays suggested an association between YTHDF1 and m6A-modified SATB1 RNA. To validate the regulatory effect of YTHDF1 on SATB1 in vivo, we established a xenograft mouse model. Knockdown of YTHDF1 significantly suppressed the growth of CNE-2R cells and downregulated SATB1 expression. Overall, our study preliminarily suggests that YTHDF1 knockdown induces tumor cell apoptosis by inhibiting the SATB1/Wnt1/β-catenin pathway, implicating YTHDF1 as a potential regulator of radiosensitivity.
PMID:
42966547
Bibliographic data and abstract were imported from PubMed on 01 Nov 2026.
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