Evidence map›Paper›PMID 37027010›Full record

ArticleMolecular cancer research : MCR2023

Tumor-Derived CCL5 Recruits Cancer-Associated Fibroblasts and Promotes Tumor Cell Proliferation in Esophageal Squamous Cell Carcinoma.

Karen J Dunbar, Tatiana A Karakasheva, Qiaosi Tang, Gizem Efe, Eric W Lin, Michael Harris, Varun Sahu, Uma M Sachdeva, Jianhua Hu, Andres J Klein-Szanto and 4 more

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Enhancing CAR-T Cell Efficacy in Solid Tumors by Inhibiting CCL5/VEGF-Mediated Angiogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
  4. Review
  5. CCL5Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Targeting cytokine and chemokine signaling pathways for cancer therapy.Signal transduction and targeted therapy · 2024
    Review
  11. Review
  12. Review
  13. Article
  14. Review
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

14 authors at 5 institutions in 1 country.

Karen J Dunbar *Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0003-0505-000X
Tatiana A Karakasheva *Gastrointestinal Epithelium Modeling Program, Division of Gastroenterology, Hepatology and Nutrition, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.ORCID 0000-0001-9070-2804
Qiaosi TangHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-6726-8728
Gizem EfeHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-1153-3326
Eric W LinGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.ORCID 0000-0002-1064-2010
Michael HarrisHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-8494-2497
Varun SahuHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-4104-9981
Uma M SachdevaHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-0442-3794
Jianhua HuHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-3306-6722
Andres J Klein-SzantoDepartment of Pathology and Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania.ORCID 0000-0002-5533-9402
Brian HenickHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0003-2681-0805
J Alan DiehlDepartment of Biochemistry, Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, Ohio.ORCID 0000-0001-9854-5049
Hiroshi NakagawaHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0001-7330-4863
Anil K RustgiHerbert Irving Comprehensive Cancer Center, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, New York.ORCID 0000-0002-6439-6919
Columbia University Irving Medical Center · USCase Western Reserve University · USChildren's Hospital of Philadelphia · USFox Chase Cancer Center · USMassachusetts General Hospital · US

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Transformed Esophageal Epithelial Cells and the Tumor MicroenvironmentP01CA098101 · NCI · UNIVERSITY OF PENNSYLVANIA · PI RUSTGI, ANIL K · 2003 to 2023
$31.7M
NCI NIH HHS P01 CA098101NCI NIH HHS P30 CA013696
6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAF) can promote tumor growth, metastasis, and therapeutic resistance in esophageal squamous cell carcinoma (ESCC), but the mechanisms of action remain elusive. Our objective was to identify secreted factor(s) that mediate the communication between CAFs and ESCC tumor cells with the aim of identifying potential druggable targets. Through unbiased cytokine arrays, we have identified CC motif chemokine ligand 5 (CCL5) as a secreted factor that is increased upon co-culture of ESCC cells and CAFs, which we replicated in esophageal adenocarcinoma (EAC) with CAFs. Loss of tumor-cell-derived CCL5 reduces ESCC cell proliferation in vitro and in vivo and we propose this is mediated, in part, by a reduction in ERK1/2 signaling. Loss of tumor-derived CCL5 reduces the percentage of CAFs recruited to xenograft tumors in vivo. CCL5 is a ligand for the CC motif receptor 5 (CCR5), for which a clinically approved inhibitor exists, namely Maraviroc. Maraviroc treatment reduced tumor volume, CAF recruitment, and ERK1/2 signaling in vivo, thus, mimicking the effects observed with genetic loss of CCL5. High CCL5 or CCR5 expression is associated with worse prognosis in low-grade esophageal carcinomas. IMPLICATIONS: These data highlight the role of CCL5 in tumorigenesis and the therapeutic potential of targeting the CCL5-CCR5 axis in ESCC.

Indexed as

Cancer-Associated FibroblastsEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsCell Line, TumorCell ProliferationChemokine CCL5ChemokinesFibroblastsHumansLigandsMaravirocCCL5 protein, humanChemokine CCL5ChemokinesLigandsMaraviroc

Identifiers

PMID37027010
PMCPMC10330279
OpenAlexW4362692795

What OpenQuestion holds

Textmetadata
LicenceTDM
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.