Evidence map›Paper›PMID 40067902›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

p53 activates circASCC3 to repress R-loops and enhance resistance to chemotherapy.

Mingming Cao, Yu Gan, Yingdan Huang, Jing Tong, Chen Xiong, Yajie Chen, Bing Chen, Ruixuan Huang, Bangxiang Xie, Jun Deng and 4 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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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

14 authors.

Mingming Cao *Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Yu Gan *Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Yingdan HuangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Jing TongFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Chen XiongFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Yajie ChenDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Bing ChenFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Ruixuan HuangDepartment of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi, China.
Bangxiang XieBeijing Institute of Hepatology, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China.
Jun DengDepartment of Oncology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi, China.
Shenglin HuangFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0003-1279-0794
Xianghuo HeFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Qian HaoFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Xiang ZhouFudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0002-1172-7948

Funding

MOST | National Natural Science Foundation of China (NSFC) 82173022MOST | National Natural Science Foundation of China (NSFC) 82273098 and 82072879
6 · The paper itself

Abstract

The tumor suppressor p53 can trigger tumor resistance to chemotherapy by facilitating DNA damage repair and maintaining genomic integrity. Here, we report that a p53-induced circular RNA circASCC3 promotes chemotherapeutic resistance by resolving R-loops. Our results reveal that p53 directly activates the transcription of

Indexed as

Drug Resistance, NeoplasmNeoplasmsR-Loop StructuresRNA, CircularTumor Suppressor Protein p53Cell Line, TumorDEAD-box RNA HelicasesDNA DamageGene Expression Regulation, NeoplasticHumansDEAD-box RNA HelicasesRNA, CircularTP53 protein, humanTumor Suppressor Protein p53chemoresistancecircular RNADDX5p53R-loop

Identifiers

PMID40067902
PMCPMC11929464

What Socratic 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 Socratic graph.