Evidence map›Paper›PMID 28986588›Full record

ArticleScientific reports2017

Autocrine DUSP28 signaling mediates pancreatic cancer malignancy via regulation of PDGF-A.

Jungwhoi Lee, Jungsul Lee, Jeong Hun Yun, Chulhee Choi, Sayeon Cho, Seung Jun Kim, Jae Hoon Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  6. International journal of molecular sciences · 2023
    Article
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  11. Pancreatic Cancer and Platelets Crosstalk: A Potential Biomarker and Target.Frontiers in cell and developmental biology · 2021
    Review
  12. Article
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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

7 authors at 4 institutions in 1 country.

Jungwhoi LeeDepartment of biotechnology, College of Applied Life Science, SARI, Jeju National University, Jeju-do, 63243, Republic of Korea. sdjd1108@kaist.ac.kr.ORCID 0000-0002-3453-0478
Jungsul LeeDepartment of Bio and Brain Engineering, KAIST, Daejeon, 34141, Republic of Korea.ORCID 0000-0002-8600-5851
Jeong Hun YunDepartment of biotechnology, College of Applied Life Science, SARI, Jeju National University, Jeju-do, 63243, Republic of Korea.
Chulhee ChoiDepartment of Bio and Brain Engineering, KAIST, Daejeon, 34141, Republic of Korea.ORCID 0000-0001-5542-9136
Sayeon ChoCollege of Pharmacy, Chung-Ang University, Seoul, 06974, Republic of Korea.
Seung Jun KimDivision of Strategic Research Planning and Assessment, Korea Research Institute of Bioscience & Biotechnology, Daejeon, 34141, Republic of Korea.
Jae Hoon KimDepartment of biotechnology, College of Applied Life Science, SARI, Jeju National University, Jeju-do, 63243, Republic of Korea. kimjh@jejunu.ac.kr.
Korea Advanced Institute of Science and Technology · KRJeju National University · KRChung-Ang University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer remains one of the most deadly cancers with a grave prognosis. Despite continuous efforts to improve remedial values, limited progress has been made. We have reported that dual specificity phosphatase 28 (DUSP28) has a critical role of chemo-resistance and migration in pancreatic cancers. However, its mechanism remains unclear. Here, we further clarify the function of DUSP28 in pancreatic cancers. Analysis using a public microarray database and in vitro assay indicated a critical role of platelet derived growth factor A (PDGF-A) in pancreatic cancer malignancy. PDGF-A was positively regulated by DUSP28 expression at the mRNA and protein levels. Enhanced DUSP28 sensitized pancreatic cancer cells to exogenous PDGF-A treatment in migration, invasion, and proliferation. Transfection with siRNA targeting DUSP28 blunted the influence of administered PDGF-A by inhibition of phosphorylation of FAK, ERK1/2, and p38 signalling pathways. In addition, DUSP28 and PDGF-A formed an acquired autonomous autocrine-signaling pathway. Furthermore, targeting DUSP28 inhibited the tumor growth and migratory features through the blockade of PDGF-A expression and intracellular signaling in vivo. Our results establish novel insight into DUSP28 and PDGF-A related autonomous signaling pathway in pancreatic cancer.

Indexed as

Autocrine CommunicationSignal TransductionAnimalsCell Line, TumorDual-Specificity PhosphatasesGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CMice, NudePancreatic NeoplasmsPlatelet-Derived Growth FactorDual-Specificity PhosphatasesPlatelet-Derived Growth Factorplatelet-derived growth factor A

Identifiers

PMID28986588
PMCPMC5630619
OpenAlexW2763293873

What OpenQuestion holds

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LicenceCC BY
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.