Evidence map›Paper›PMID 28795470›Full record

ArticleCancer science2017

Dermokine contributes to epithelial-mesenchymal transition through increased activation of signal transducer and activator of transcription 3 in pancreatic cancer.

Chaohao Huang, Yukai Xiang, Shengchuan Chen, Huajun Yu, Zhengde Wen, Tingting Ye, Hongwei Sun, Hongru Kong, Dapei Li, Dinglai Yu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Chaohao HuangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID http://orcid.org/0000-0001-7292-7866
Yukai XiangDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Shengchuan ChenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Huajun YuDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Zhengde WenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Tingting YeDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Hongwei SunDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Hongru KongDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Dapei LiSuzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Suzhou, China.
Dinglai YuDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Bicheng ChenDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Mengtao ZhouDepartment of Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNWenzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dermokine (DMKN) was first identified in relation to skin lesion healing and skin carcinoma. Recently, its expression was associated with pancreatic cancer tumorigenesis, although its involvement remains poorly understood. Herein, we showed that DMKN loss of function in Patu-8988 and PANC-1 pancreatic cancer cell lines resulted in reduced phosphorylation of signal transducer and activator of transcription 3, and increased activation of ERK1/2 and AKT serine/threonine kinase. This decreased the proliferation ability of pancreatic ductal adenocarcinoma (PDAC) cells. In addition, DMKN knockdown decreased the invasion and migration of PDAC cells, partially reversed the epithelial-mesenchymal transition, retarded tumor growth in a xenograft animal model by decreasing the density of microvessels, and attenuated the distant metastasis of human PDAC in a mouse model. Taken together, these data suggested that DMKN could be a potential prognostic biomarker and therapeutic target in pancreatic cancer.

Indexed as

AnimalsBiomarkers, TumorCarcinogenesisCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Knockdown TechniquesHumansIntercellular Signaling Peptides and ProteinsMiceNeoplasm InvasivenessNeoplasm MetastasisPancreatic NeoplasmsProteinsSTAT3 Transcription FactorXenograft Model Antitumor AssaysBiomarkers, TumorDMKN protein, humanIntercellular Signaling Peptides and ProteinsProteinsSTAT3 protein, humanSTAT3 Transcription FactorAngiogenesisDMKNepithelial-mesenchymal transitionpancreatic ductal adenocarcinomaSTAT3

Identifiers

PMID28795470
PMCPMC5665845
OpenAlexW2745178996

What OpenQuestion holds

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LicenceCC BY-NC
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.