Evidence map›Paper›PMID 35902640›Full record

ArticleBritish journal of cancer2022

Neuropeptide Y, a paracrine factor secreted by cancer cells, is an independent regulator of angiogenesis in colon cancer.

Debanjan Chakroborty, Sandeep Goswami, Hao Fan, Wendy L Frankel, Sujit Basu, Chandrani Sarkar

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2022. 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
3.7field-weighted citation impact, top 6% 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, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Neuropeptide Y as a Neuro-Immune Checkpoint in Cancer.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
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  13. Neuropeptide Y Peptide Family and Cancer: Antitumor Therapeutic Strategies.International journal of molecular sciences · 2023
    Review
  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

6 authors at 2 institutions in 1 country.

Debanjan Chakroborty *Department of Pathology, The Ohio State University, Columbus, OH, 43210, USA.
Sandeep Goswami *Department of Pathology, The Ohio State University, Columbus, OH, 43210, USA.
Hao FanDepartment of Pathology, The Ohio State University, Columbus, OH, 43210, USA.
Wendy L FrankelDepartment of Pathology, The Ohio State University, Columbus, OH, 43210, USA.
Sujit BasuDepartment of Pathology, The Ohio State University, Columbus, OH, 43210, USA.
Chandrani SarkarDepartment of Pathology, The Ohio State University, Columbus, OH, 43210, USA. csarkar@southalabama.edu.ORCID http://orcid.org/0000-0001-7143-8278
The Ohio State University · USUSA Mitchell Cancer Institute · US

Funding

Development of a novel antiangiogenic drug for colon cancer by targeting neuropeptide Y receptorsR21CA216763 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SARKAR, CHANDRANI · 2018 to 2019
$368k
NCI NIH HHS R21 CA216763
6 · The paper itself

Abstract

backgroundResistance to anti-angiogenic therapies targeting vascular endothelial growth factor-A (VEGF-A) stems from VEGF-A independent angiogenesis mediated by other proangiogenic factors. Therefore identifying these factors in colon adenocarcinoma (CA) will reveal new therapeutic targets.

methodsNeuropeptide Y (NPY) and Y2 receptor (Y2R) expressions in CA were studied by immunohistochemical analysis. Orthotopic HT29 with intact VEGF-A gene and VEGF-A knockdown (by CRISPR/Cas9 gene-editing technique) HT29 colon cancer-bearing mice were treated with specific Y2R antagonists, and the effects on angiogenesis and tumour growth were studied. The direct effect of NPY on angiogenesis and the underlying molecular mechanism was elucidated by the modulation of Y2R receptors expressed on colonic endothelial cells (CEC).

resultsThe results demonstrated that NPY and Y2R are overexpressed in human CA, orthotopic HT29, and most interestingly in VEGF-A-depleted orthotopic HT29 tumours. Treatment with Y2R antagonists inhibited angiogenesis and thereby HT29 tumour growth. Blocking /silencing Y2R abrogated NPY-induced angiogenic potential of CEC. Mechanistically, NPY regulated the activation of the ERK/MAPK signalling pathway in CEC.

conclusionsNPY derived from cancer cells independently regulates angiogenesis in CA by acting through Y2R present on CEC. Targeting NPY/Y2R thus emerges as a novel potential therapeutic strategy in CA.

Indexed as

AdenocarcinomaColonic NeoplasmsAnimalsEndothelial CellsHumansMiceNeovascularization, PathologicNeuropeptide YVascular Endothelial Growth Factor ANeuropeptide YVascular Endothelial Growth Factor A

Identifiers

PMID35902640
PMCPMC9553928
OpenAlexW4288077185

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.