Evidence map›Paper›PMID 33414393›Full record

ArticleCell death & disease2021

Cell-cycle arrest and senescence in TP53-wild type renal carcinoma by enhancer RNA-P53-bound enhancer regions 2 (p53BER2) in a p53-dependent pathway.

Haibiao Xie, Kaifang Ma, Kenan Zhang, Jingcheng Zhou, Lei Li, Wuping Yang, Yanqing Gong, Lin Cai, Kan Gong

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
10.5field-weighted citation impact, top 1% of its field
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

33 citing papers in PubMed, 156 citations in OpenAlex.

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  20. The impact of hypoxia on extracellular vesicle secretome profile of cancer.Medical oncology (Northwood, London, England) · 2023
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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

9 authors at 1 institution in 1 country.

Haibiao XieDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China.
Kaifang MaDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China.
Kenan ZhangDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China.
Jingcheng ZhouDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China.ORCID 0000-0002-6226-5667
Lei LiDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China.
Wuping YangDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China.
Yanqing GongDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China. yqgong@bjmu.edu.cn.
Lin CaiDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China. drcailin@163.com.
Kan GongDepartment of Urology, Peking University First Hospital, Beijing, People's Republic of China. gongkan_pku@126.com.ORCID 0000-0001-7195-677X
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TP53 is a classic tumor suppressor, but its role in kidney cancer remains unclear. In our study, we tried to explain the role of p53 in kidney cancer through the p53-related enhancer RNA pathway. Functional experiments were used to explore whether P53-bound enhancer regions 2 (p53BER2) has a role in the cell cycle and senescence response of TP53-wild type (WT) renal cancer cells in vitro or vivo. RNA-sequencing was used to identify the potential target of p53BER2. The results showed that the expression level of P53BER2 was downregulated in renal cancer tissues and cell lines, further dual-luciferase experiments and APR-256-reactivated experiments showed p53BER2 expresses in a p53-dependent way. Moreover, knockdown p53BER2 could reverse nutlin-3-induced cytotoxic effect in TP53-WT cell lines. Further exploration showed the downregulation of p53BER2 could reverse nutlin-3-induced G1-arrest and senescence in TP53-WT cell lines. What is more, the knockdown of p53BER2 showed resistance to nutlin-3 treatment in vivo. Additionally, we found BRCA2 could be regulated by p53BER2 in vitro and vivo; further experiment showed p53BER2 could induce cell-cycle arrest and DNA repair by mediating BRCA2. In summary, the p53-associated enhancer RNA-p53BER2 mediates the cell cycle and senescence of p53 in TP53-WT renal cancer cells.

Indexed as

AnimalsBiomarkers, TumorCarcinoma, Renal CellCell Cycle CheckpointsCell ProliferationHumansKidney NeoplasmsMaleMiceMice, NudeMiddle AgedTransfectionTumor Suppressor Protein p53Biomarkers, TumorTumor Suppressor Protein p53

Identifiers

PMID33414393
PMCPMC7791070
OpenAlexW3111404439

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.