Evidence map›Paper›PMID 41604083›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

Akt/mTOR pathway-mediated CCNA1 regulation of radiotherapy resistance in nasopharyngeal carcinoma.

Ruifang Zeng, Liting Zhong, Pengfei Li, Xiaoying Gao, Yanfeng Chen, Wenwen Hao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Ruifang Zeng *Department of Cancer Center, Southern Medical University Hospital of Integrated Traditional Chinese and Western Medicine, Southern Medical University, Guangzhou, 510315, China.
Liting Zhong *Department of VIP Region, The Ethics Committee of the Zhongshan Ophthalmic Center of Sun Yat-Sen University, Guangzhou, 510060, China.
Pengfei Li *Department of Cancer Center, Southern Medical University Hospital of Integrated Traditional Chinese and Western Medicine, Southern Medical University, Guangzhou, 510315, China.
Xiaoying GaoDepartment of Cancer Center, Southern Medical University Hospital of Integrated Traditional Chinese and Western Medicine, Southern Medical University, Guangzhou, 510315, China.
Yanfeng ChenState Key Laboratory of Oncology in South China, Department of Head and Neck Surgery, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China. chenyf@sysucc.org.cn.
Wenwen HaoDepartment of Cancer Center, Southern Medical University Hospital of Integrated Traditional Chinese and Western Medicine, Southern Medical University, Guangzhou, 510315, China. 297781938@qq.com.

Funding

Guangdong Hong Kong Macao University Alliance Fund GWLM20252008Guangdong Medical Science and Technology Research Fund A2024755Medical Research Foundation of Guangdong Province A2025005Natural Science Foundation of Guangdong Province 2021A1515010602Science and Technology Plan Project of Guangzhou City 2025A04J4087Special Fund for Major R&D of China National Health Commission (2021KYSHX01508Traditional Chinese Medicine Bureau of Guangdong Province 20232077
6 · The paper itself

Abstract

backgroundNasopharyngeal carcinoma (NPC), as a cancer type highly sensitive to radiotherapy, has radiation therapy as the preferred clinical treatment strategy. However, acquired radioresistance poses a significant challenge to the overall therapeutic efficacy for NPC patients.

methodsIn this study, we established two radioresistant NPC cell lines, CNE2-IR and HONE1-IR.

resultsRNA sequencing analysis revealed that CCNA1 was upregulated in both radioresistant NPC cell lines. Downregulation of CCNA1 enhanced the radiosensitivity of these two radioresistant NPC cell lines. Further research found that CCNA1 expression was induced and upregulated during radiotherapy and was associated with poor prognosis in NPC patients. Through in-depth mechanistic studies, we confirmed that CCNA1 may influence radiosensitivity through ROS antioxidant stress and anti-apoptotic signaling. High expression of CCNA1 enhanced NPC cell viability and inhibited apoptosis, while downregulating CCNA1 improved the radiosensitivity of NPC cells. The mechanism of radiosensitization was primarily mediated by the AKT/mTOR pathway.

conclusionsThese findings suggest that CCNA1 could serve as a potential predictive biomarker for radiosensitivity in NPC patients, providing new insights for developing personalized comprehensive chemoradiotherapy strategies for NPC patients.

Indexed as

Nasopharyngeal CarcinomaNasopharyngeal NeoplasmsProto-Oncogene Proteins c-aktRadiation ToleranceSignal TransductionTOR Serine-Threonine KinasesApoptosisCarcinomaCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHumansReactive Oxygen SpeciesMTOR protein, humanProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine KinasesAkt/mTORCCNA1NPCRadioresistanceROS

Identifiers

PMID41604083
PMCPMC12852267

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LicenceCC BY-NC-ND
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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.