Evidence map›Paper›PMID 28986450›Full record

ArticleThe Journal of biological chemistry2017

STAP-2 protein promotes prostate cancer growth by enhancing epidermal growth factor receptor stabilization.

Yuichi Kitai, Masashi Iwakami, Kodai Saitoh, Sumihito Togi, Serina Isayama, Yuichi Sekine, Ryuta Muromoto, Jun-Ichi Kashiwakura, Akihiko Yoshimura, Kenji Oritani and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. STAP2 promotes the progression of renal fibrosis via HSP27.Journal of translational medicine · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. SH2 Domains: Folding, Binding and Therapeutical Approaches.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. 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

11 authors at 3 institutions in 1 country.

Yuichi KitaiFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Masashi IwakamiFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Kodai SaitohFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Sumihito TogiFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Serina IsayamaFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Yuichi SekineFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Ryuta MuromotoFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Jun-Ichi KashiwakuraFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812.
Akihiko Yoshimurathe the Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, and.
Kenji Oritanithe Department of Hematology, International University of Health and Welfare, 4-3 Kouzunomori, Narita, Chiba 286-8686, Japan.
Tadashi MatsudaFrom the Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-Ku, Sapporo, Hokkaido 060-0812, tmatsuda@pharm.hokudai.ac.jp.
Hokkaido University · JPInternational University of Health and Welfare · JPKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signal-transducing adaptor family member-2 (STAP-2) is an adaptor protein that regulates various intracellular signaling pathways and promotes tumorigenesis in melanoma and breast cancer cells. However, the contribution of STAP-2 to the behavior of other types of cancer cells is unclear. Here, we show that STAP-2 promotes tumorigenesis of prostate cancer cells through up-regulation of EGF receptor (EGFR) signaling. Tumor growth of a prostate cancer cell line, DU145, was strongly decreased by STAP-2 knockdown. EGF-induced gene expression and phosphorylation of AKT, ERK, and STAT3 were significantly decreased in STAP-2-knockdown DU145 cells. Mechanistically, we found that STAP-2 interacted with EGFR and enhanced its stability by inhibiting c-CBL-mediated EGFR ubiquitination. Our results indicate that STAP-2 promotes prostate cancer progression via facilitating EGFR activation.

Indexed as

Cell ProliferationAdaptor Proteins, Signal TransducingAnimalsErbB ReceptorsHumansMaleMice, Inbred BALB CPhosphoproteinsPhosphorylationProstatic NeoplasmsProtein StabilitySignal TransductionTumor Cells, CulturedUbiquitinationXenograft Model Antitumor AssaysAdaptor Proteins, Signal TransducingEGFR protein, humanErbB ReceptorsPhosphoproteinsSTAP2 protein, humanadaptor proteinc-CBLprostate cancerprotein degradationsignal transductionSTAT3

Identifiers

PMID28986450
PMCPMC5702677
OpenAlexW2763690609

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.