Evidence map›Paper›PMID 31847880›Full record

ArticleJournal of hematology & oncology2019

Endothelial-mesenchymal transition harnesses HSP90α-secreting M2-macrophages to exacerbate pancreatic ductal adenocarcinoma.

Chi-Shuan Fan, Li-Li Chen, Tsu-An Hsu, Chia-Chi Chen, Kee Voon Chua, Chung-Pin Li, Tze-Sing Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 20% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.

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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 3 institutions in 1 country.

Chi-Shuan FanNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Township, 350, Miaoli, Taiwan.
Li-Li ChenNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Township, 350, Miaoli, Taiwan.
Tsu-An HsuInstitute of Biotechnology and Pharmaceutical Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Township, 350, Miaoli, Taiwan.
Chia-Chi ChenNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Township, 350, Miaoli, Taiwan.
Kee Voon ChuaNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Township, 350, Miaoli, Taiwan.
Chung-Pin LiDivision of Gastroenterology and Hepatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Tze-Sing HuangNational Institute of Cancer Research, National Health Research Institutes, No. 35, Keyan Road, Zhunan Township, 350, Miaoli, Taiwan. tshuang@nhri.org.tw.ORCID 0000-0001-8736-4330
National Health Research Institutes · TWKaohsiung Medical University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial-to-mesenchymal transition (EndoMT) can provide a source of cancer-associated fibroblasts which contribute to desmoplasia of many malignancies including pancreatic ductal adenocarcinoma (PDAC). We investigated the clinical relevance of EndoMT in PDAC, and explored its underlying mechanism and therapeutic implication.

methodsExpression levels of 29 long non-coding RNAs were analyzed from the cells undergoing EndoMT, and an EndoMT index was proposed to survey its clinical associations in the PDAC patients of The Cancer Genome Atlas database. The observed clinical correlation was further confirmed by a mouse model inoculated with EndoMT cells-involved PDAC cell grafts. In vitro co-culture with EndoMT cells or treatment with the conditioned medium were performed to explore the underlying mechanism. Because secreted HSP90α was involved, anti-HSP90α antibody was evaluated for its inhibitory efficacy against the EndoMT-involved PDAC tumor.

resultsA combination of low expressions of LOC340340, LOC101927256, and MNX1-AS1 was used as an EndoMT index. The clinical PDAC tissues with positive EndoMT index were significantly correlated with T4-staging and showed positive for M2-macrophage index. Our mouse model and in vitro cell-culture experiments revealed that HSP90α secreted by EndoMT cells could induce macrophage M2-polarization and more HSP90α secretion to promote PDAC tumor growth. Furthermore, anti-HSP90α antibody showed a potent therapeutic efficacy against the EndoMT and M2-macrophages-involved PDAC tumor growth.

conclusionsEndoMT cells can secrete HSP90α to harness HSP90α-overproducing M2-type macrophages to promote PDAC tumor growth, and such effect can be targeted and abolished by anti-HSP90α antibody.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsApoptosisBiomarkers, TumorCarcinoma, Pancreatic DuctalCell MovementCell ProliferationEndothelium, VascularGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansMacrophagesMiceMice, Inbred C57BLPancreatic NeoplasmsTumor Cells, CulturedBiomarkers, TumorHSP90AA2P protein, humanHSP90 Heat-Shock ProteinsCancer-associated fibroblasteHSP90αEndoMTM2-type macrophage

Identifiers

PMID31847880
PMCPMC6918594
OpenAlexW2994907128

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.