Evidence map›Paper›PMID 29701272›Full record

ArticleCell proliferation2018

dCK negatively regulates the NRF2/ARE axis and ROS production in pancreatic cancer.

Qiangsheng Hu, Yi Qin, Jinfeng Xiang, Wensheng Liu, Wenyan Xu, Qiqing Sun, Shunrong Ji, Jiang Liu, Zheng Zhang, Quanxing Ni and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 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

13 authors at 1 institution in 1 country.

Qiangsheng HuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Yi QinDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Jinfeng XiangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Wensheng LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Wenyan XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Qiqing SunDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Shunrong JiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Jiang LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Zheng ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Quanxing NiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.ORCID http://orcid.org/0000-0002-6697-7143
Bo ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Shanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDecreased deoxycytidine kinase (dCK) expression is a reported indicator of gemcitabine efficacy in pancreatic cancer, due to the impact of this kinase on gemcitabine metabolism. The transcription factor NF-E2 p45-related factor 2 (NRF2, also called Nfe2l2), a master regulator of redox homoeostasis, has been reported to tightly control the expression of numerous ROS-detoxification genes and participates in drug resistance. However, the contribution of dCK to the NRF2 signalling axis has seldom been discussed and needs investigation. MATERIALS AND

methodsBy overexpressing dCK in pancreatic cancer cells, we assessed the impact of dCK on NRF2 transcriptional activity. Furthermore, we measured the impact of dCK expression on the intracellular redox balance and reactive oxygen species (ROS) production. By utilizing immunohistochemical staining and tissues from pancreatic cancer patients, we assessed the correlation between dCK and NRF2 expression. Through proliferation and metastasis assays, we examined the impact of dCK expression on cell proliferation and metastasis.

resultsdCK negatively regulates NRF2 transcriptional activity, leading to the decreased expression of ARE-driven antioxidant genes. In addition, dCK negatively regulates intracellular redox homoeostasis and ROS production. Negative correlations between dCK and NRF2 levels in pancreatic cancer cell lines and patient samples were observed. In vitro cell line studies suggested that dCK negatively regulated proliferation and metastasis.

conclusionDecreased dCK expression promotes NRF2-driven antioxidant transcription, which further enhances gemcitabine treatment resistance, forming a feedback loop.

Indexed as

AcetylcysteineCell Line, TumorCell ProliferationCell SurvivalDeoxycytidineDeoxycytidine KinaseDrug Resistance, NeoplasmGemcitabineGlutamate-Cysteine LigaseGlutathioneHumansKelch-Like ECH-Associated Protein 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-E2-Related Factor 2Pancreatic NeoplasmsAcetylcysteineDeoxycytidineDeoxycytidine KinaseGCLC protein, humanGemcitabineGlutamate-Cysteine LigaseGlutathioneKelch-Like ECH-Associated Protein 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-E2-Related Factor 2Reactive Oxygen SpeciesAREdCKgemcitabineNRF2pancreatic cancerROS

Identifiers

PMID29701272
PMCPMC6528851
OpenAlexW2801785540

What OpenQuestion holds

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LicenceCC BY
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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.