E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance

Abstract Oral squamous cell carcinoma (OSCC) is a frequently occurring neck and head malignancy. Therapies for OSCC are improving, but radiotherapy resistance remains a major clinical challenge. Here, we found that the S-phase kinase-associated protein 2 (Skp2) is overexpressed in OSCC cells and tis...

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Main Authors: Shiming Tan, Ruirui Wang, Jinglin Fang, Ming Yi, Pengfei Guo, Shuangze Han, Xiaoying Li, Yu Gan, Jinzhuang Liao, Xinfang Yu, Wei Li
Format: Article
Language:English
Published: Nature Publishing Group 2025-04-01
Series:Cell Death Discovery
Online Access:https://doi.org/10.1038/s41420-025-02463-3
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author Shiming Tan
Ruirui Wang
Jinglin Fang
Ming Yi
Pengfei Guo
Shuangze Han
Xiaoying Li
Yu Gan
Jinzhuang Liao
Xinfang Yu
Wei Li
author_facet Shiming Tan
Ruirui Wang
Jinglin Fang
Ming Yi
Pengfei Guo
Shuangze Han
Xiaoying Li
Yu Gan
Jinzhuang Liao
Xinfang Yu
Wei Li
author_sort Shiming Tan
collection DOAJ
description Abstract Oral squamous cell carcinoma (OSCC) is a frequently occurring neck and head malignancy. Therapies for OSCC are improving, but radiotherapy resistance remains a major clinical challenge. Here, we found that the S-phase kinase-associated protein 2 (Skp2) is overexpressed in OSCC cells and tissues. Knockdown of Skp2 significantly increased the radiotherapy sensitivity of OSCC cells. Further potential mechanisms suggest that Skp2-deficient restoration of radiotherapy sensitivity in OSCC cells may induce intrinsic apoptosis through inhibition of the Akt/Wee1/CDK1 axis, which inhibits Survivin phosphorylation and promotes its ubiquitination and degradation by FBXL7. Clinicopathologic histological analysis showed that Skp2 was positively correlated with the expression of p-Akt and Survivin in OSCC tissues. Furthermore, knockdown or inhibition of Skp2 overcame the radiotherapy resistance of OSCC cells. In conclusion, our study demonstrated that targeting the Skp2-Survivin axis could serve as an attractive and promising potential therapeutic target for radiotherapy sensitization in OSCC.
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issn 2058-7716
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publisher Nature Publishing Group
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series Cell Death Discovery
spelling doaj-art-d062c2c0b9cc4c148ed96c21c8977c8c2025-08-20T02:11:58ZengNature Publishing GroupCell Death Discovery2058-77162025-04-0111111510.1038/s41420-025-02463-3E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistanceShiming Tan0Ruirui Wang1Jinglin Fang2Ming Yi3Pengfei Guo4Shuangze Han5Xiaoying Li6Yu Gan7Jinzhuang Liao8Xinfang Yu9Wei Li10Department of Radiology, The Third Xiangya Hospital of Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversitySchool of Stomatology Hunan University of Chinese MedicineDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, XiangYa Hospital, Central South UniversityDepartment of Radiology, The Third Xiangya Hospital of Central South UniversityAbstract Oral squamous cell carcinoma (OSCC) is a frequently occurring neck and head malignancy. Therapies for OSCC are improving, but radiotherapy resistance remains a major clinical challenge. Here, we found that the S-phase kinase-associated protein 2 (Skp2) is overexpressed in OSCC cells and tissues. Knockdown of Skp2 significantly increased the radiotherapy sensitivity of OSCC cells. Further potential mechanisms suggest that Skp2-deficient restoration of radiotherapy sensitivity in OSCC cells may induce intrinsic apoptosis through inhibition of the Akt/Wee1/CDK1 axis, which inhibits Survivin phosphorylation and promotes its ubiquitination and degradation by FBXL7. Clinicopathologic histological analysis showed that Skp2 was positively correlated with the expression of p-Akt and Survivin in OSCC tissues. Furthermore, knockdown or inhibition of Skp2 overcame the radiotherapy resistance of OSCC cells. In conclusion, our study demonstrated that targeting the Skp2-Survivin axis could serve as an attractive and promising potential therapeutic target for radiotherapy sensitization in OSCC.https://doi.org/10.1038/s41420-025-02463-3
spellingShingle Shiming Tan
Ruirui Wang
Jinglin Fang
Ming Yi
Pengfei Guo
Shuangze Han
Xiaoying Li
Yu Gan
Jinzhuang Liao
Xinfang Yu
Wei Li
E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance
Cell Death Discovery
title E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance
title_full E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance
title_fullStr E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance
title_full_unstemmed E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance
title_short E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance
title_sort e3 ligase skp2 mediated stabilization of survivin contributes to radioresistance
url https://doi.org/10.1038/s41420-025-02463-3
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