Evidence map›Paper›PMID 26804165›Full record

ArticleOncogene2016

GEP oncogene promotes cell proliferation through YAP activation in ovarian cancer.

H Yagi, K Asanoma, T Ohgami, A Ichinoe, K Sonoda, K Kato

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. GαFrontiers in cell and developmental biology · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Naturally occurring hotspot cancer mutations in GαThe Journal of biological chemistry · 2020
    Article
  12. Review
  13. Article
  14. The HIPPO pathway in gynecological malignancies.American journal of cancer research · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Signaling mechanisms and physiological functions of G-protein GαProtein science : a publication of the Protein Society · 2019
    Review
  19. Article
  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

6 authors at 1 institution in 1 country.

H YagiDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
K AsanomaDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
T OhgamiDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
A IchinoeDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
K SonodaDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
K KatoDepartment of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G-protein-coupled receptors (GPCRs) and their ligands function in the progression of human malignancies. Gα12 and Gα13, encoded by GNA12 and GNA13, respectively, are referred to as the GEP oncogene and are implicated in tumor progression. However, the molecular mechanisms by which Gα12/13 activation promotes cancer progression are not fully elucidated. Here, we demonstrate elevated expression of Gα12/13 in human ovarian cancer tissues. Gα12/13 activation did not promote cellular migration in the ovarian cancer cell lines examined. Rather, Gα12/13 activation promoted cell growth. We used a synthetic biology approach using chimeric G proteins and GPCRs activated solely by artificial ligands to selectively trigger signaling pathways downstream of specific G proteins. We found that Gα12/13 promotes proliferation of ovarian cancer cells by activating the transcriptional coactivator YAP, a critical component of the Hippo signaling pathway. Furthermore, we reveal that inhibition of YAP by short hairpin RNA or a specific inhibitor prevented the growth of ovarian cancer cells. Therefore, YAP may be a suitable therapeutic target in ovarian cancer.

Indexed as

Cell ProliferationOncogenesActive Transport, Cell NucleusAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorFemaleGTP-Binding Protein alpha Subunits, G12-G13Hippo Signaling PathwayHumansMiceMice, Inbred BALB COvarian NeoplasmsPhosphoproteinsPhosphorylationProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingGTP-Binding Protein alpha Subunits, G12-G13LATS1 protein, humanPhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID26804165
OpenAlexW2273342883

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.