Evidence map›Paper›PMID 24833309›Full record

ArticleScientific reports2014

Pancreatic tumor cell secreted CCN1/Cyr61 promotes endothelial cell migration and aberrant neovascularization.

Gargi Maity, Smita Mehta, Inamul Haque, Kakali Dhar, Sandipto Sarkar, Sushanta K Banerjee, Snigdha Banerjee

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

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  12. Polymer nanoparticle-assisted chemotherapy of pancreatic cancer.Therapeutic advances in medical oncology · 2020
    Review
  13. Article
  14. Aspirin suppresses tumor cell-induced angiogenesis and their incongruity.Journal of cell communication and signaling · 2019
    Article
  15. Article
  16. Article
  17. Review
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  20. Identification ofGenetics · 2018
    Article
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

7 authors at 1 institution in 1 country.

Gargi Maity1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2] Division of Hematology and Oncology, University of Kansas Medical Center, Kansas City, Kansas [3].
Smita Mehta1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2].
Inamul Haque1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2] Division of Hematology and Oncology, University of Kansas Medical Center, Kansas City, Kansas.
Kakali Dhar1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2].
Sandipto Sarkar1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2] Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, Kansas.
Sushanta K Banerjee1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2] Division of Hematology and Oncology, University of Kansas Medical Center, Kansas City, Kansas [3] Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, Kansas [4] Department of Pathology, University of Kansas Medical Center, Kansas City, Kansas.
Snigdha Banerjee1] Cancer Research Unit, Kansas City VA Medical Center, Kansas City, MO [2] Division of Hematology and Oncology, University of Kansas Medical Center, Kansas City, Kansas.
University of Kansas · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
The Role of CCN5 in Progression of Breast CancerI01BX001989 · VA · KANSAS CITY VA MEDICAL CENTER · PI BANERJEE, SUSHANTA K. · 2013 to 2016
–
BLRD VA I01 BX001989NCATS NIH HHS UL1 TR000077NCATS NIH HHS UL1 TR001425
6 · The paper itself

Abstract

The complex signaling networks between cancer cells and adjacent endothelial cells make it challenging to unravel how cancer cells send extracellular messages to promote aberrant vascularization or tumor angiogenesis. Here, in vitro and in vivo models show that pancreatic cancer cell generated unique microenvironments can underlie endothelial cell migration and tumor angiogenesis. Mechanistically, we find that pancreatic cancer cell secreted CCN1/Cyr61 matricellular protein rewires the microenvironment to promote endothelial cell migration and tumor angiogenesis. This event can be overcome by Sonic Hedgehog (SHh) antibody treatment. Collectively, these studies identify a novel CCN1 signaling program in pancreatic cancer cells which activates SHh through autocrine-paracrine circuits to promote endothelial cell migration and tumor angiogenesis and suggests that CCN1 signaling of pancreatic cancer cells is vital for the regulation of tumor angiogenesis. Thus CCN1 signaling could be an ideal target for tumor vascular disruption in pancreatic cancer.

Indexed as

AnimalsCell LineCell Line, TumorCell MovementCysteine-Rich Protein 61Endothelial CellsEndothelium, VascularHedgehog ProteinsHumansMiceNeovascularization, PathologicPancreatic NeoplasmsSignal TransductionTumor MicroenvironmentCysteine-Rich Protein 61Hedgehog Proteins

Identifiers

PMID24833309
PMCPMC4023131
OpenAlexW1990755427

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.