Evidence map›Paper›PMID 36548277›Full record

ArticlePloS one2022

Notch signaling regulates vasculogenic mimicry and promotes cell morphogenesis and the epithelial-to-mesenchymal transition in pancreatic ductal adenocarcinoma.

Nontawat Benjakul, Nattapa Prakobphol, Chayada Tangshewinsirikul, Wirada Dulyaphat, Jisnuson Svasti, Komgrid Charngkaew, Thaned Kangsamaksin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
1.4field-weighted citation impact, top 19% 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, 18 citations in OpenAlex.

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  6. Murine Cell Line Models for Vascular Mimicry: The Role of YAP/TAZ Signaling.International journal of molecular sciences · 2025
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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

7 authors at 2 institutions in 1 country.

Nontawat BenjakulFaculty of Medicine Siriraj Hospital, Department of Pathology, Mahidol University, Bangkok, Thailand.ORCID 0000-0002-6198-2752
Nattapa PrakobpholFaculty of Science, Department of Biochemistry, Mahidol University, Bangkok, Thailand.
Chayada TangshewinsirikulFaculty of Medicine Ramathibodi Hospital, Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Mahidol University, Bangkok, Thailand.
Wirada DulyaphatFaculty of Medicine Ramathibodi Hospital, Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Mahidol University, Bangkok, Thailand.ORCID 0000-0002-1758-8563
Jisnuson SvastiFaculty of Science, Department of Biochemistry, Mahidol University, Bangkok, Thailand.
Komgrid CharngkaewFaculty of Medicine Siriraj Hospital, Department of Pathology, Mahidol University, Bangkok, Thailand.
Thaned KangsamaksinFaculty of Science, Department of Biochemistry, Mahidol University, Bangkok, Thailand.ORCID 0000-0002-3497-1791
Mahidol University · THSiriraj Hospital · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vasculogenic mimicry (VM) is the process where cancer cells adopt endothelial characteristics by forming tube-like structures and perfusing channels. This phenomenon has been demonstrated in several types of solid tumors and associated with the growth and survival of tumor cells. In this study, we investigated the presence of VM formation in human pancreatic ductal adenocarcinoma (PDAC) and elucidated the molecular mechanisms underlying the VM process. In human PDAC tissues, CD31-negative, periodic acid-Schiff (PAS)-positive channels were predominantly found in desmoplastic areas, which are generally also hypovascularized. We found a positive correlation of VM capacity to tumor size and NOTCH1 expression and nuclear localization with statistical significance, implicating that Notch activity is involved with VM formation. Additionally, our data showed that the presence of growth or angiogenic factors significantly increased Notch activity in PDAC cell lines and upregulated several mesenchymal marker genes, such as TWIST1 and SNAI1, which can be inhibited by a gamma-secretase inhibitor. Our data showed that Notch signaling plays an important role in inducing VM formation in PDAC by promoting the epithelial-to-mesenchymal transition process.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsCell Line, TumorEpithelial-Mesenchymal TransitionHumansMorphogenesisNeovascularization, Pathologic

Identifiers

PMID36548277
PMCPMC9779037
OpenAlexW4312091461

What OpenQuestion holds

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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.