Evidence map›Paper›PMID 27345410›Full record

ArticleOncogene2017

PTPRO represses ERBB2-driven breast oncogenesis by dephosphorylation and endosomal internalization of ERBB2.

H Dong, L Ma, J Gan, W Lin, C Chen, Z Yao, L Du, L Zheng, C Ke, X Huang and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-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

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Tumor-Associated Macrophage in Breast Tumor Microenvironment.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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 5 institutions in 2 countries.

H DongCancer Research Center, Shantou University Medical College, Shantou, China.
L MaDepartment of Gastroenterology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
J GanCancer Research Center, Shantou University Medical College, Shantou, China.
W LinCancer Research Center, Shantou University Medical College, Shantou, China.
C ChenCancer Research Center, Shantou University Medical College, Shantou, China.
Z YaoCancer Research Center, Shantou University Medical College, Shantou, China.
L DuCancer Research Center, Shantou University Medical College, Shantou, China.
L ZhengCancer Research Center, Shantou University Medical College, Shantou, China.
C KeCancer Research Center, Shantou University Medical College, Shantou, China.
X HuangMOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China.
H SongDepartment of Cell Biology, Xi'an Jiaotong University Suzhou Academy, Suzhou, China.
R KumarDepartment of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, George Washington University, Washington DC, USA.
S C YeungCancer Research Center, Shantou University Medical College, Shantou, China.
H ZhangCancer Research Center, Shantou University Medical College, Shantou, China.
Shantou University · CNShantou University Medical College · CNGeorge Washington University · USModel Animal Research Center · CNXi’an Jiaotong-Liverpool University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The plasma membrane-associated tyrosine phosphatase PTPRO is frequently transcriptionally repressed in cancers and signifies poor prognosis of breast cancer patients. In this study, deletion of Ptpro in MMTV-Erbb2 transgenic mice dramatically shortened the mammary tumor latency and accelerated tumor growth due to loss of Ptpro within the breast cancer cells but not in surrounding tissue as confirmed by hetero-transplantation studies. Both in vitro and in vivo data demonstrated that the phosphatase activity was required for the inactivation of ERBB2 and its downstream signaling. PTPRO regulated the phosphorylation status of ERBB2 at Y1248. Co-immunoprecipitation and proximity ligation assay (Duolink) indicated that PTPRO directly physically interacted with ERBB2. Moreover, PTPRO phosphatase activity shortened the half-life of ERBB2 by increasing endocytotic degradation. PTPRO reexpression by demethylation treatment using 5-azacytidine reduced the proliferation and colony formation potential in ERBB2-positive breast cancer cells. Taken together, PTPRO inhibited ERBB2-driven breast cancer through dephosphorylation leading to dual effects of ERBB2 signaling suppression and endosomal internalization of ERBB2, Therefore, reexpression of PTPRO may be a potential therapy for ERBB2-overexpressing breast cancer.

Indexed as

AnimalsCell ProliferationEndosomesErb-b2 Receptor Tyrosine KinasesFemaleHumansMammary Neoplasms, ExperimentalMice, TransgenicPhosphorylationReceptor-Like Protein Tyrosine Phosphatases, Class 3Signal TransductionTyrosineERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesPTPRO protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 3Tyrosine

Identifiers

PMID27345410
PMCPMC5269534
OpenAlexW2466900436

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.