Evidence map›Paper›PMID 28260059›Full record

ArticleOncology reports2017

EPAC1 overexpression is a prognostic marker and its inhibition shows promising therapeutic potential for gastric cancer.

Ding-Ping Sun, Chia-Lang Fang, Han-Kun Chen, Kuo-Shan Wen, You-Cheng Hseu, Shih-Ting Hung, Yih-Huei Uen, Kai-Yuan Lin

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Function of mCancer biology & therapy · 2023
    Article
  7. Article
  8. Review
  9. Review
  10. The LncRNA DUXAP10 Could Function as a Promising Oncogene in Human Cancer.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. The Role of Epac in Cancer Progression.International journal of molecular sciences · 2020
    Review
  13. Selective small-molecule EPAC activators.Biochemical Society transactions · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

8 authors at 1 institution in 1 country.

Ding-Ping SunDepartment of Surgery, Chi Mei Medical Center, Tainan, Taiwan, R.O.C.
Chia-Lang FangDepartment of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C.
Han-Kun ChenDepartment of Surgery, Chi Mei Medical Center, Tainan, Taiwan, R.O.C.
Kuo-Shan WenDepartment of Pharmacy, Chi Mei Medical Center, Tainan, Taiwan, R.O.C.
You-Cheng HseuDepartment of Cosmeceutics, China Medical University, Taichung, Taiwan, R.O.C.
Shih-Ting HungDepartment of Medical Research, Chi Mei Medical Center, Tainan, Taiwan, R.O.C.
Yih-Huei UenThe Superintendent's Office, Chi Mei Hospital Chiali, Tainan, Taiwan, R.O.C.
Kai-Yuan LinDepartment of Medical Research, Chi Mei Medical Center, Tainan, Taiwan, R.O.C.
China Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

cAMP signaling controls a variety of cellular functions. In addition to the well-known signal transducer cAMP-dependent protein kinase, a more recently discovered transducer is the exchange protein directly activated by cAMP (EPAC). EPAC responses are mediated by small G proteins, which regulate biologic functions such as cell adhesion, migration and proliferation. Recently, the clinical importance of EPAC1 has received increased attention. This study investigated the correlations between the expression of EPAC1 and various clinicopathologic parameters as well as the survival of the patients with gastric cancer (GC). The patient cohort in this study consisted of 141 cases of GC that presented from 1999 through 2011; documented clinicopathologic parameters and clinical outcomes were available for all cases. Immunoblotting, immunohistochemistry and quantitative real-time PCR were used to examine EPAC1 expression in gastric cells and tissues. siRNA technology was used to study the effect of EPAC1 knockdown on cell proliferation and invasion. An increase in EPAC1 expression was found in GC cells and tissues. The overexpression of EPAC1 was associated with the depth of invasion (P=0.0021), stage (P=0.0429), and vascular invasion (P=0.0049) and was correlated with poor disease-free survival (P=0.0029) and overall survival (P=0.0024). A univariate Cox regression analysis showed that the overexpression of EPAC1 was a prognostic marker for GC (P=0.038). Furthermore, cell studies indicated that the knockdown of EPAC1 in GC cells suppressed cell proliferation and invasion. The overexpression of EPAC1 can be used as a marker to predict the outcome of patients with GC, and EPAC1 represents a potential therapeutic modality for treating GC.

Indexed as

PrognosisAgedCell Line, TumorCell ProliferationCyclic AMPDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGuanine Nucleotide Exchange FactorsHumansMaleMiddle AgedNeoplasm InvasivenessProportional Hazards ModelsSignal TransductionCyclic AMPGuanine Nucleotide Exchange FactorsRAPGEF3 protein, human

Identifiers

PMID28260059
PMCPMC5367365
OpenAlexW2587838322

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Registered trials

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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.