Evidence map›Paper›PMID 28148261›Full record

ArticleMolecular cancer2017

Dclk1, a tumor stem cell marker, regulates pro-survival signaling and self-renewal of intestinal tumor cells.

Parthasarathy Chandrakesan, Jiannan Yao, Dongfeng Qu, Randal May, Nathaniel Weygant, Yang Ge, Naushad Ali, Sripathi M Sureban, Modhi Gude, Kenneth Vega and 5 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 122 citations in OpenAlex.

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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 2 countries.

Parthasarathy ChandrakesanDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA. parthasarathy-chandrakesan@ouhsc.edu.ORCID 0000-0002-7587-9553
Jiannan YaoDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Dongfeng QuDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Randal MayDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Nathaniel WeygantDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Yang GeDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Naushad AliDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Sripathi M SurebanDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Modhi GudeDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Kenneth VegaDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Eddie Bannerman-MensonCOARE Biotechnology, Oklahoma City, OK, USA.
Lijun XiaOklahoma Medical Research Foundation, Oklahoma City, OK, USA.
Michael BronzeDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Guangyu AnBeijing Chao-Yang Hospital Department of Oncology, Capital Medical University, Beijing, China. anguangyu@hotmail.com.
Courtney W HouchenDivision of Digestive Diseases and Nutrition, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA. Courtney-houchen@ouhsc.edu.
University of Oklahoma Health Sciences Center · USCapital Medical University · CNVeterans Health Administration · USCoare Biotechnology (United States) · USDiabetes & Endocrine Associates · USNational Jewish Health · USOklahoma Medical Research Foundation · US

Funding

Intestinal Stem Cell Consortium Coordinating CenterU01DK085532 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NILAND, JOYCE CAROL · 2009 to 2018
$6.5M
Role of Mucin-type O-glycans in Intestinal InflammationR01DK085691 · NIDDK · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI David Casero, Lijun Xia · 2010 to 2026
$6.2M
Limited Competition for the Continuation of the Intestinal Stem Cell Consortium Coordinating CenterU24DK085532 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NILAND, JOYCE CAROL · 2019 to 2023
$2.3M
Isolation and Characterization of Intestinal Stem Cells Using Novel Markers (RP)U01DK085508 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI HOUCHEN, COURTNEY WAYNE · 2009 to 2014
$2.0M
NIDDK NIH HHS U01 DK085508NIDDK NIH HHS U01 DK085532NIDDK NIH HHS U24 DK085532
6 · The paper itself

Abstract

backgroundMore than 80% of intestinal neoplasia is associated with the adenomatous polyposis coli (APC) mutation. Doublecortin-like kinase 1 (Dclk1), a kinase protein, is overexpressed in colorectal cancer and specifically marks tumor stem cells (TSCs) that self-renew and increased the tumor progeny in Apc

methodsWe analyzed DCLK1 and pro-survival signaling gene expression datasets of 329 specimens from TCGA Colon Adenocarcinoma Cancer Data. The network of DCLK1 and pro-survival signaling was analyzed utilizing the GeneMANIA database. We examined the expression levels of Dclk1 and other stem cell-associated markers, pro-survival signaling pathways, cell self-renewal in the isolated intestinal epithelial cells of Apc

resultsWe found a correlation between DCLK1 and pro-survival signaling expression. The expression of Dclk1 and stem cell-associated markers Lgr5, Bmi1, and Musashi1 were significantly higher in the intestinal epithelial cells of Apc

conclusionOur results indicate that Dclk1 is essential in advancing intestinal tumorigenesis. Knocking down Dclk1 decreases tumor stemness and progression and is thus predicted to regulate pro-survival signaling and tumor cell pluripotency. This study provides a strong rationale to target Dclk1 as a treatment strategy for colorectal cancer.

Indexed as

Signal TransductionAdenocarcinomaAnimalsCell Self RenewalCell SurvivalCluster AnalysisColonic NeoplasmsDisease Models, AnimalDoublecortin-Like KinasesEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Knockdown TechniquesGenes, APCHumansIntracellular Signaling Peptides and ProteinsDCLK1 protein, humanDoublecortin-Like KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesReceptor, Notch1APC mutationCancer stem cellsColorectal cancerDclk1Intestinal epithelial cellsNanoparticlesPro-survival signalingSelf-renewal

Identifiers

PMID28148261
PMCPMC5286867
OpenAlexW2583546331

What OpenQuestion holds

Textmetadata
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.