Evidence map›Paper›PMID 40195315›Full record

ArticleCell death discovery2025

E3 ligase Skp2-mediated stabilization of survivin contributes to radioresistance.

Shiming Tan, Ruirui Wang, Jinglin Fang, Ming Yi, Pengfei Guo, Shuangze Han, Xiaoying Li, Yu Gan, Jinzhuang Liao, Xinfang Yu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Shiming TanDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Ruirui WangDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Jinglin FangSchool of Stomatology Hunan University of Chinese Medicine, Changsha, China.
Ming YiDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Pengfei GuoDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Shuangze HanDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Xiaoying LiDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.ORCID http://orcid.org/0000-0001-6541-064X
Yu GanDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.
Jinzhuang LiaoDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China.ORCID http://orcid.org/0000-0002-8377-8269
Xinfang YuKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, XiangYa Hospital, Central South University, Changsha, China.
Wei LiDepartment of Radiology, The Third Xiangya Hospital of Central South University, Changsha, China. weililx@csu.edu.cn.ORCID http://orcid.org/0000-0002-7267-6494

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Identifiers

PMID40195315
PMCPMC11977269

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.