Evidence map›Paper›PMID 23995790›Full record

ArticleOncogene2014

CKIP-1 acts as a colonic tumor suppressor by repressing oncogenic Smurf1 synthesis and promoting Smurf1 autodegradation.

J Nie, L Liu, G Xing, M Zhang, R Wei, M Guo, X Li, P Xie, L Li, F He and 2 more

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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, 38 citations in OpenAlex.

  1. Trial
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  4. Review
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  8. High expression of theThe Journal of international medical research · 2020
    Article
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  10. Article
  11. Upregulation ofCell & bioscience · 2019
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

J Nie1] Department of Molecular Biology, Institute of Basic Medicine, PLA General Hospital, Beijing, China [2] State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
L LiuDepartment of General Surgery, PLA General Hospital, Beijing, China.
G XingState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
M ZhangState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
R Wei1] State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China [2] School of Life Sciences, Tsinghua University, Beijing, China.
M GuoDepartment of Gastroenterology and Hepatology, PLA General Hospital, Beijing, China.
X LiDepartment of Molecular Biology, Institute of Basic Medicine, PLA General Hospital, Beijing, China.
P XieState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
L LiState Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China.
F He1] State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China [2] School of Life Sciences, Tsinghua University, Beijing, China.
W HanDepartment of Molecular Biology, Institute of Basic Medicine, PLA General Hospital, Beijing, China.
L Zhang1] State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing, China [2] Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.
Beijing Proteome Research Center · CNChinese PLA General Hospital · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of cellular signaling pathways can lead to colon cancer. However, research on the key signaling effectors or regulators in colon carcinogenesis is limited. Casein kinase-2 interacting protein-1 (CKIP-1; also known as PLEKHO1) is crucial during adult bone formation and is a promising drug target for osteoporosis therapy. In this study, we observed that CKIP-1 was downregulated in human colon cancer tissues and colon cancer cell lines, and this result was correlated with colon cancer progression. CKIP-1 silencing in colon cancers involved promoter methylation. In colon cancer HCT116 and SW480 cells, CKIP-1 overexpression inhibited cell growth and migration. CKIP-1 also suppressed in-vivo tumor formation. Notably, the growth-suppressive role of CKIP-1 was dependent on the downregulation of the cell cycle-regulated oncogene Smad ubiquitylation regulatory factor-1 (Smurf1). During cell cycle progression, phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling increased Smurf1 production by an mTOR-dependent translational control mechanism. Rapamycin, the mTOR inhibitor, significantly reduced Smurf1 protein levels, and Smurf1 was degraded in mitosis. In colon cancer, CKIP-1 controlled Smurf1 expression by suppressing PI3K/Akt/mTOR signaling and enhancing Smurf1 autodegradation, and CKIP-1 downregulation was correlated with Smurf1 upregulation in colon carcinogenesis. These findings provide novel insight into the mechanisms of the candidate tumor suppressor CKIP-1.

Indexed as

ProteolysisAnimalsCarrier ProteinsCell CycleCell Line, TumorCell ProliferationColonic NeoplasmsDisease ProgressionDNA MethylationFemaleGene Expression Regulation, NeoplasticGene SilencingIntracellular Signaling Peptides and ProteinsMicePromoter Regions, GeneticTOR Serine-Threonine KinasesCarrier ProteinsIntracellular Signaling Peptides and ProteinsPLEKHO1 protein, humanSMURF1 protein, humanTOR Serine-Threonine KinasesTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID23995790
OpenAlexW2614508755

What OpenQuestion holds

Textmetadata
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.