Evidence map›Paper›PMID 33945523›Full record

ArticlePLoS genetics2021

CBFB cooperates with p53 to maintain TAp73 expression and suppress breast cancer.

Navdeep Malik, Hualong Yan, Howard H Yang, Gamze Ayaz, Wendy DuBois, Yu-Chou Tseng, Young-Im Kim, Shunlin Jiang, Chengyu Liu, Maxwell Lee and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021
    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 at 2 institutions in 1 country.

Navdeep MalikCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.ORCID 0000-0003-1113-2562
Hualong YanCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Howard H YangHigh-Dimension Data Analysis Group, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.ORCID 0000-0002-9291-631X
Gamze AyazCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Wendy DuBoisCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Yu-Chou TsengCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.ORCID 0000-0002-2832-255X
Young-Im KimCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Shunlin JiangCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Chengyu LiuTransgenic Core, National Heart, Lung, and Blood Institute, Bethesda, Maryland, United States of America.
Maxwell LeeHigh-Dimension Data Analysis Group, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.
Jing HuangCancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America.ORCID 0000-0002-7163-5156
National Cancer Institute · USNational Heart Lung and Blood Institute · US

Funding

Transgenic CoreZICHL005907 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LIU, CHENGYU · 2010 to 2025
$25.8M
Animal Model and Genotyping Core Support FacilityZICBC011047 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DU BOIS DE VROYLANDE, WENDY · 2009 to 2025
$23.1M
Vulnerabilities in osteosarcoma and breast cancerZIABC011504 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUANG, JING · 2013 to 2025
$13.3M
Integrated analyses of genetics, epigenetics, and gene expressionZIHBC011703 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI LEE, MAXWELL · 2016 to 2025
$10.9M
The roles of p53 in embryonic stem cellsZIABC011158 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HUANG, JING · 2009 to 2023
$8.4M
Intramural NIH HHS ZIA BC011158Intramural NIH HHS ZIA BC011504
6 · The paper itself

Abstract

The CBFB gene is frequently mutated in several types of solid tumors. Emerging evidence suggests that CBFB is a tumor suppressor in breast cancer. However, our understanding of the tumor suppressive function of CBFB remains incomplete. Here, we analyze genetic interactions between mutations of CBFB and other highly mutated genes in human breast cancer datasets and find that CBFB and TP53 mutations are mutually exclusive, suggesting a functional association between CBFB and p53. Integrated genomic studies reveal that TAp73 is a common transcriptional target of CBFB and p53. CBFB cooperates with p53 to maintain TAp73 expression, as either CBFB or p53 loss leads to TAp73 depletion. TAp73 re-expression abrogates the tumorigenic effect of CBFB deletion. Although TAp73 loss alone is insufficient for tumorigenesis, it enhances the tumorigenic effect of NOTCH3 overexpression, a downstream event of CBFB loss. Immunohistochemistry shows that p73 loss is coupled with higher proliferation in xenografts. Moreover, TAp73 loss-of-expression is a frequent event in human breast cancer tumors and cell lines. Together, our results significantly advance our understanding of the tumor suppressive functions of CBFB and reveal a mechanism underlying the communication between the two tumor suppressors CBFB and p53.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell Transformation, NeoplasticCore Binding Factor Alpha 2 SubunitCore Binding Factor beta SubunitFemaleGenes, Tumor SuppressorHumansImmunohistochemistryMiceMutationReceptor, Notch3Transcription, GeneticCBFB protein, humanCore Binding Factor Alpha 2 SubunitCore Binding Factor beta SubunitNOTCH3 protein, humanReceptor, Notch3RUNX1 protein, humanTP53 protein, humanTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53

Identifiers

PMID33945523
PMCPMC8121313
OpenAlexW3159727437

What OpenQuestion holds

Textmetadata
LicenceCC0
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.