Evidence map›Paper›PMID 30459355›Full record

ArticleOncogene2019

Oncogenic activity of poly (ADP-ribose) glycohydrolase.

Maud Marques, Maika Jangal, Li-Chun Wang, Anna Kazanets, Sabrina Daniela da Silva, Tiejun Zhao, Amanda Lovato, Henry Yu, Su Jie, Sonia Del Rincon and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Poly (ADP-Ribose) Glycohydrolase-Dependent dePARylation of PCNA Is Essential for DNA Replication.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Prospects for PARG inhibitors in cancer therapy.Journal of molecular cell biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

14 authors at 3 institutions in 1 country.

Maud MarquesDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Maika JangalDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Li-Chun WangDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Anna KazanetsDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Sabrina Daniela da SilvaDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Tiejun ZhaoDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Amanda LovatoDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Henry YuDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Su JieDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Sonia Del RinconDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
John MackeyDepartment of Oncology, Division of Medical Oncology, Cross Cancer Institute, University of Alberta, Edmonton, AB, Canada.
Sambasivarao DamarajuDepartment of Laboratory Medicine and Pathology, Cross Cancer Institute, University of Alberta, Edmonton, AB, Canada.
Moulay Alaoui-JamaliDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada.
Michael WitcherDepartments of Oncology and Experimental Medicine, The Lady Davis Institute of the Jewish General Hospital, McGill University, Montreal, QC, Canada. Michael.Witcher@mcgill.ca.
Jewish General Hospital · CAMcGill University · CAUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly (ADP-ribosylation), known as PARylation, is a post-translational modification catalyzed by poly (ADP-ribose) polymerases (PARP) and primarily removed by the enzyme poly (ADP-ribose) glycohydrolase (PARG). While the aberrant removal of post-translation modifications including phosphorylation and methylation has known tumorigenic effects, deregulation of PARylation has not been widely studied. Increased hydrolysis of PARylation chains facilitates cancer growth through enhancing estrogen receptor (ER)-driven proliferation, but oncogenic transformation has not been linked to increased PARG expression. In this study, we find that elevated PARG levels are associated with a poor prognosis in breast cancers, especially in HER2-positive and triple-negative subtypes. Using both in vitro and in vivo models, we demonstrate that heightened expression of catalytically active PARG facilitates cell transformation and invasion of normal mammary epithelial cells. Catalytically inactive PARG mutants did not recapitulate these phenotypes. Consistent with clinical data showing elevated PARG predicts poor outcomes in HER2+ patients, we observed that PARG acts in synergy with HER2 to promote neoplastic growth of immortalized mammary cells. In contrast, PARG depletion significantly impairs the growth and metastasis of triple-negative breast tumors. Mechanistically, we find that PARG interacts with SMAD2/3 and significantly decreases their PARylation in non-transformed cells, leading to enhanced expression of SMAD target genes. Further linking SMAD-mediated transcription to the oncogenicity of PARG, we show that PARG-mediated anchorage-independent growth and invasion are dependent, at least in part, on SMAD expression. Overall, our study underscores the oncogenic impact of aberrant protein PARylation and highlights the therapeutic potential of PARG inhibition in breast cancer.

Indexed as

CarcinogenesisAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell Transformation, NeoplasticDNAEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGlycoside HydrolasesHumansMiceNeoplasm MetastasisPhenotypeSmad2 ProteinDNAGlycoside Hydrolasespoly ADP-ribose glycohydrolaseSmad2 ProteinSmad3 Protein

Identifiers

PMID30459355
PMCPMC6484711
OpenAlexW2900836368

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.