Evidence map›Paper›PMID 23435421›Full record

ArticleOncogene2014

PTPN12 promotes resistance to oxidative stress and supports tumorigenesis by regulating FOXO signaling.

I S Harris, H Blaser, J Moreno, A E Treloar, C Gorrini, M Sasaki, J M Mason, C B Knobbe, A Rufini, M Hallé and 6 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Alterations in Sod2-Induced Oxidative Stress Affect Endocrine Cancer Progression.The Journal of clinical endocrinology and metabolism · 2018
    Article
  12. Article
  13. Mitochondrial ROS control of cancer.Seminars in cancer biology · 2017
    Review
  14. Article
  15. Article
  16. Correlation between Oxidative Stress, Nutrition, and Cancer Initiation.International journal of molecular sciences · 2017
    Review
  17. Article
  18. Review
  19. Review
  20. Article
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

16 authors at 5 institutions in 2 countries.

I S Harris1] The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
H BlaserThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
J Moreno1] The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada [2] Laboratory Medicine Program, University Health Network, Toronto, Ontario, Canada [3] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
A E TreloarThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
C GorriniThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
M SasakiThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
J M MasonThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
C B Knobbe1] The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Neuropathology, Heinrich Heine University, Düsseldorf, Germany.
A RufiniLaboratory of Apoptosis in Cancer, MRC Toxicology Unit, University of Leicester, Leicester, UK.
M HalléDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, Quebec, Canada.
A J EliaThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
A WakehamThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
M L TremblayDepartment of Biochemistry, Rosalind and Morris Goodman Cancer Centre, McGill University, Montreal, Quebec, Canada.
G MelinoLaboratory of Apoptosis in Cancer, MRC Toxicology Unit, University of Leicester, Leicester, UK.
S Done1] The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada [3] Laboratory Medicine Program, University Health Network, Toronto, Ontario, Canada [4] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
T W Mak1] The Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
University Health Network · CAPrincess Margaret Cancer Centre · CAMcGill University Health Centre · CAMRC Toxicology Unit · GBUniversity of Leicester · GB

Funding

CIHRMedical Research Council MC_U132670600
6 · The paper itself

Abstract

It is well known that protein tyrosine phosphatases (PTPs) that become oxidized due to exposure to reactive oxygen species (ROS) undergo a conformational change and are inactivated. However, whether PTPs can actively regulate ROS levels in order to prevent PTP inhibition has yet to be investigated. Here, we demonstrate that PTP non-receptor type 12 (PTPN12) protects cells against aberrant ROS accumulation and death induced by oxidative stress. Murine embryonic fibroblasts (MEFs) deficient in PTPN12 underwent increased ROS-induced apoptosis under conditions of antioxidant depletion. Cells lacking PTPN12 also showed defective activation of FOXO1/3a, transcription factors required for the upregulation of several antioxidant genes. PTPN12-mediated regulation of ROS appeared to be mediated by phosphoinositide-dependent kinase-1 (PDK1), which was hyperstimulated in the absence of PTPN12. As tight regulation of ROS to sustain survival is a key feature of cancer cells, we examined PTPN12 levels in tumors from a cohort of breast cancer patients. Patients whose tumors showed high levels of PTPN12 transcripts had a significantly poorer prognosis. Analysis of tissues from patients with various breast cancer subtypes revealed that more triple-negative breast cancers, the most aggressive breast cancer subtype, showed high PTPN12 expression than any other subtype. Furthermore, both human breast cancer cells and mouse mammary epithelial tumor cells engineered to lack PTPN12 exhibited reduced tumorigenic and metastatic potential in vivo that correlated with their elevated ROS levels. The involvement of PTPN12 in the antioxidant response of breast cancer cells suggests that PTPN12 may represent a novel therapeutic target for this disease.

Indexed as

Oxidative StressSignal TransductionAnimalsBreast NeoplasmsCell DivisionCells, CulturedFemaleForkhead Transcription FactorsHumansMicePrognosisProtein Tyrosine Phosphatase, Non-Receptor Type 12Reactive Oxygen SpeciesReal-Time Polymerase Chain ReactionRNA, MessengerForkhead Transcription FactorsProtein Tyrosine Phosphatase, Non-Receptor Type 12PTPN12 protein, humanReactive Oxygen SpeciesRNA, Messenger

Identifiers

PMID23435421
OpenAlexW1997509856

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.