Evidence map›Paper›PMID 30738331›Full record

ArticleNeoplasia (New York, N.Y.)2019

Disrupting Inflammation-Associated CXCL8-CXCR1 Signaling Inhibits Tumorigenicity Initiated by Sporadic- and Colitis-Colon Cancer Stem Cells.

Robert C Fisher, Kishan Bellamkonda, L Alex Molina, Shao Xiang, David Liska, Samaneh K Sarvestani, Susmita Chakrabarti, Annamarie Berg, Marda L Jorgensen, Denise Hatala and 5 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 36 citations in OpenAlex.

  1. Interleukin-8 in health and disease.Molecular biomedicine · 2026
    Review
  2. Article
  3. Phytochemical Analysis and Anticancer Activity ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Mechanistic Insights into Tumorigenesis from Serum Proteins.medRxiv : the preprint server for health sciences · 2025
    Article
  6. Article
  7. Article
  8. Review
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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

15 authors at 5 institutions in 1 country.

Robert C FisherDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Kishan BellamkondaDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
L Alex MolinaDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Shao XiangDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
David LiskaDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Colorectal Surgery, Cleveland Clinic, Cleveland, OH, USA.
Samaneh K SarvestaniDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Susmita ChakrabartiDepartment of Molecular Cardiology, Cleveland Clinic, Cleveland, OH, USA.
Annamarie BergDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Marda L JorgensenDepartment of Pediatrics, University of Florida, Gainesville, Florida, USA.
Denise HatalaImmunochemistry Core, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.
Sugong ChenDepartment of Surgery, Duke University Medical Center, Durham, North Carolina, USA.
Alexandra AielloQuantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA.
Henry D AppelmanDepartment of Pathology, University of Michigan, Ann Arbor, MI, USA.
Edward W ScottDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, Florida, USA.
Emina H HuangDepartment of Stem Cell Biology and Regenerative Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Colorectal Surgery, Cleveland Clinic, Cleveland, OH, USA. Electronic address: huange2@ccf.org.
Cleveland Clinic Lerner College of Medicine · USCleveland Clinic · USUniversity of Florida · USDuke Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

An organotypic model recapitulating colon cancer microenvironment and metastasisU01CA214300 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HUANG, EMINA HUI-NA, SHEN, XILING · 2017 to 2021
$3.1M
The role of IL8 in colitis-associated tumor initiationR01CA157663 · NCI · UNIVERSITY OF FLORIDA · PI HUANG, EMINA HUI-NA · 2012 to 2016
$1.6M
The role of the colitic stem cell niche in oncogenesisR01CA142808 · NCI · UNIVERSITY OF FLORIDA · PI HUANG, EMINA HUI-NA · 2010 to 2014
$1.5M
Axolotl Hematopoiesis: A Regeneration ModelR01DK105916 · NIDDK · UNIVERSITY OF FLORIDA · PI SCOTT, EDWARD W · 2015 to 2018
$1.4M
NCI NIH HHS R01 CA142808NCI NIH HHS R01 CA157663NCI NIH HHS U01 CA214300NIDDK NIH HHS R01 DK105916
6 · The paper itself

Abstract

Dysfunctional inflammatory pathways are associated with an increased risk of cancer, including colorectal cancer. We have previously identified and enriched for a self-renewing, colon cancer stem cell (CCSC) subpopulation in primary sporadic colorectal cancers (CRC) and a related subpopulation in ulcerative colitis (UC) patients defined by the stem cell marker, aldehyde dehydrogenase (ALDH). Subsequent work demonstrated that CCSC-initiated tumors are dependent on the inflammatory chemokine, CXCL8, a known inducer of tumor proliferation, angiogenesis and invasion. Here, we use RNA interference to target CXCL8 and its receptor, CXCR1, to establish the existence of a functional signaling pathway promoting tumor growth initiated by sporadic and colitis CCSCs. Knocking down either CXCL8 or CXCR1 had a dramatic effect on inhibiting both in vitro proliferation and angiogenesis. Likewise, tumorigenicity was significantly inhibited due to reduced levels of proliferation and angiogenesis. Decreased expression of cycle cell regulators cyclins D1 and B1 along with increased p21 levels suggested that the reduction in tumor growth is due to dysregulation of cell cycle progression. Therapeutically targeting the CXCL8-CXCR1 signaling pathway has the potential to block sustained tumorigenesis by inhibiting both CCSC- and pCCSC-induced proliferation and angiogenesis.

Indexed as

Signal TransductionAnimalsBiomarkersCell Line, TumorCell ProliferationCell Transformation, NeoplasticColitisColonic NeoplasmsDisease Models, AnimalGene DosageGene ExpressionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansImmunophenotypingBiomarkersCXCL8 protein, humanInterleukin-8Receptors, Interleukin-8A

Identifiers

PMID30738331
PMCPMC6370871
OpenAlexW2914914225

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.