Evidence map›Paper›PMID 28975366›Full record

ReviewCellular and molecular life sciences : CMLS2018

A double dealing tale of p63: an oncogene or a tumor suppressor.

Yonglong Chen, Yougong Peng, Shijie Fan, Yimin Li, Zhi-Xiong Xiao, Chenghua Li

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 73 citations in OpenAlex.

  1. WWOX maintains epidermal identity and suppresses EMT to prevent aggressive cutaneous squamous cell carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  18. Polymorphism in theAfrican health sciences · 2021
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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

6 authors at 2 institutions in 1 country.

Yonglong ChenCenter of Growth, Metabolism and Aging, Key Laboratory of Biological Resources and Ecological Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610065, China.
Yougong PengDepartment of General Surgery, The Second People's Hospital of Jingmen, Jingmen, 448000, China.
Shijie FanCenter of Growth, Metabolism and Aging, Key Laboratory of Biological Resources and Ecological Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610065, China.
Yimin LiCenter of Growth, Metabolism and Aging, Key Laboratory of Biological Resources and Ecological Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610065, China.
Zhi-Xiong XiaoCenter of Growth, Metabolism and Aging, Key Laboratory of Biological Resources and Ecological Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610065, China.
Chenghua LiCenter of Growth, Metabolism and Aging, Key Laboratory of Biological Resources and Ecological Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, 610065, China. lichenghua@scu.edu.cn.ORCID 0000-0001-7096-6845
Sichuan University · CNFirst People’s Hospital of Jingmen · CN

Funding

Department of Science and Technology of Sichuan Province (CN) #2016JY0152National Natural Science Foundation of China #31671423
6 · The paper itself

Abstract

As a member of tumor suppressor p53 family, p63, a gene encoding versatile protein variant, has been documented to correlate with cancer formation and progression, though it is rarely mutated in cancer patients. However, it has long been controversial on whether p63 is an oncogene or a tumor suppressor. Here, we comprehensively reviewed reports on roles of p63 in development, tumorigenesis and tumor progression. According to data from molecular cell biology, genetic models and clinic research, we conclude that p63 may act as either an oncogene or a tumor suppressor gene in different scenarios: TA isoforms of p63 gene are generally tumor-suppressive through repressing cell proliferation, survival and metastasis; ΔN isoforms, however, may initiate tumorigenesis via promoting cell proliferation and survival, but inhibit tumor metastasis and progression; effects of p63 on tumor formation and progression depend on the context of the whole p53 family, and either amplification or loss of p63 gene locus can break the balance to cause tumorigenesis.

Indexed as

Gene Expression Regulation, NeoplasticApoptosis Regulatory ProteinsCarcinogenesisCell ProliferationCell SurvivalDNA-Binding ProteinsHumansNeoplasmsPhosphoproteinsProtein IsoformsSignal TransductionTrans-ActivatorsTranscription FactorsTumor Suppressor ProteinsApoptosis Regulatory ProteinsDNA-Binding ProteinsPhosphoproteinsProtein IsoformsTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor ProteinsCell migrationCell senescenceOncoproteinTAp63ΔNp63

Identifiers

PMID28975366
PMCPMC11105324
OpenAlexW2763474643

What OpenQuestion holds

Textmetadata
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.