Evidence map›Paper›PMID 26956429›Full record

ArticleeLife2016

Transglutaminase 2 contributes to a TP53-induced autophagy program to prevent oncogenic transformation.

Shi Yun Yeo, Yoko Itahana, Alvin Kunyao Guo, Rachel Han, Kozue Iwamoto, Hung Thanh Nguyen, Yi Bao, Kai Kleiber, Ya Jun Wu, Boon Huat Bay and 2 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
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  5. Advancements inMolecules (Basel, Switzerland) · 2024
    Review
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  19. Article
  20. Emerging Roles of p53 Family Members in Glucose Metabolism.International journal of molecular sciences · 2018
    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

12 authors at 2 institutions in 1 country.

Shi Yun YeoCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Yoko ItahanaCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Alvin Kunyao GuoCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Rachel HanCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Kozue IwamotoCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Hung Thanh NguyenCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Yi BaoCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Kai KleiberCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Ya Jun WuDepartment of Anatomy, Yong Loo Lin School of Medicine, National University Health System, , Singapore.
Boon Huat BayDepartment of Anatomy, Yong Loo Lin School of Medicine, National University Health System, , Singapore.
Mathijs VoorhoeveCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.
Koji ItahanaCancer & Stem Cell Biology Program, Duke-NUS Medical School, , Singapore.ORCID http://orcid.org/0000-0002-7241-2894
Duke-NUS Medical School · SGNational University Health System · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic alterations which impair the function of the TP53 signaling pathway in TP53 wild-type human tumors remain elusive. To identify new components of this pathway, we performed a screen for genes whose loss-of-function debilitated TP53 signaling and enabled oncogenic transformation of human mammary epithelial cells. We identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway. TGM2 suppressed colony formation in soft agar and tumor formation in a xenograft mouse model. The depletion of growth supplements induced both TGM2 expression and autophagy in a TP53-dependent manner, and TGM2 promoted autophagic flux by enhancing autophagic protein degradation and autolysosome clearance. Reduced expression of both CDKN1A, which regulates the cell cycle downstream of TP53, and TGM2 synergized to promote oncogenic transformation. Our findings suggest that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two important barriers in the TP53 pathway that prevent oncogenic transformation.

Indexed as

AutophagyCell Transformation, NeoplasticAnimalsEpithelial CellsGenetic TestingGTP-Binding ProteinsHeterograftsHumansMammary Neoplasms, ExperimentalMiceProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesTumor Suppressor Protein p53GTP-Binding ProteinsProtein Glutamine gamma Glutamyltransferase 2TGM2 protein, humanTP53 protein, humanTransglutaminasesTumor Suppressor Protein p53autophagyCDKN1Achromosomesgeneshumanhuman biologymedicinemouseoncogenic transformationTGM2TP53

Identifiers

PMID26956429
PMCPMC4798945
OpenAlexW2296606837

What OpenQuestion 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 OpenQuestion graph.