Evidence map›Paper›PMID 29343851›Full record

ArticleOncogene2018

NDRG2 facilitates colorectal cancer differentiation through the regulation of Skp2-p21/p27 axis.

Liangliang Shen, Xuan Qu, Huichen Li, Chunsheng Xu, Mengying Wei, Qinhao Wang, Yi Ru, Bei Liu, Yuqiao Xu, Kai Li and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

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  13. TheInternational journal of molecular sciences · 2023
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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

20 authors at 5 institutions in 1 country.

Liangliang ShenThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China. bioliangshen@fmmu.edu.cn.
Xuan QuShaanxi University of Chinese Medicine, Xianyang, China.
Huichen LiThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Chunsheng XuDepartment of General Surgery, No.537 Hospital of PLA, Baoji, China.
Mengying WeiThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Qinhao WangThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Yi RuThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Bei LiuDepartment of Neurosurgery and Institute for Functional Brain Disorders, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.
Yuqiao XuThe State Key Laboratory of Cancer Biology and Department of Pathology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Kai LiDepartment of Clinical Laboratory, General Hospital of Xinjiang Military Command, Xinjiang, China.
Junbi HuDepartment of Gastroenterology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Lifeng WangThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Yongzheng MaThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Mengyang LiThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Xiaofeng LaiThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Lei GaoDepartment of Urology, Wuhan General Hospital of Guangzhou Military Region, Wuhan, Hubei, China.
Kaichun WuState Key Laboratory of Cancer Biology, National Clinical Research Center for Digestive Diseases and Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, China.
Libo YaoThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.
Jianyong ZhengState Key Laboratory of Cancer Biology, Department of Gastrointestinal Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. zhjy68@163.com.
Jian ZhangThe State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China. biozhangj@fmmu.edu.cn.
Air Force Medical University · CNXijing Hospital · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNShaanxi University of Chinese Medicine · CNWuhan General Hospital of Guangzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poorly differentiated colorectal cancers (CRCs) are more aggressive and lack targeted therapies. We and others previously reported the predominant role of tumor-suppressor NDRG2 in promoting CRC differentiation, but the underlying mechanism is largely unknown. Herein, we demonstrate that NDRG2 induction of CRC cell differentiation is dependent on the repression of E3 ligase Skp2 activity. In patients and Ndrg2 knockout mice, NDRG2 and Skp2 are negatively correlated and associated with cell differentiation stage. Further, NDRG2 suppression of Skp2 contributes to the inductions and stabilizations of p21 and p27, which are Skp2 target proteins for degradation. The reduction of either p21 or p27 levels by shRNA can decrease NDRG2-induced AKP activity and resume cell growth inhibition, thus both p21 and p27 are required for NDRG2 effect on the promotion of cell differentiation in CRCs. The mechanistic study shows that NDRG2 suppresses β-catenin nuclear translocation and decreases the occupancy of β-catenin/TCF complex on Skp2 promoter, potentially through dephosphorylating GSK-3β. By subjecting a series of NDRG2 deletion mutants to Skp2 expression, the loss of NH

Indexed as

AdenocarcinomaAnimalsBiomarkers, TumorCaco-2 CellsCell DifferentiationCell ProliferationColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Gene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansIntestinal MucosaMaleMiceBiomarkers, TumorCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27NDRG2 protein, humanSKP2 protein, humanS-Phase Kinase-Associated ProteinsTumor Suppressor Proteins

Identifiers

PMID29343851
PMCPMC5874257
OpenAlexW2783718453

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.