Evidence map›Paper›PMID 31836008›Full record

ArticleBMC cancer2019

TIMP-2 secreted by monocyte-like cells is a potent suppressor of invadopodia formation in pancreatic cancer cells.

Christian Benzing, Hoyin Lam, Chi Man Tsang, Alexander Rimmer, Yoana Arroyo-Berdugo, Yolanda Calle, Claire M Wells

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  6. The TIMP protein family: diverse roles in pathophysiology.American journal of physiology. Cell physiology · 2024
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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 3 countries.

Christian BenzingSchool of Cancer and Pharmaceutical Sciences, New Hunts House, Kings College London, London, SE1 1UL, UK.
Hoyin LamSchool of Cancer and Pharmaceutical Sciences, New Hunts House, Kings College London, London, SE1 1UL, UK.
Chi Man TsangDepartment of Anatomical and Cellular Pathology and State Key Laboratory of Translational Oncology, The Chinese University of Hong Kong, Hongkong, Hong Kong SAR.
Alexander RimmerSchool of Cancer and Pharmaceutical Sciences, New Hunts House, Kings College London, London, SE1 1UL, UK.
Yoana Arroyo-BerdugoDepartment of Life Sciences, University of Roehampton, London, UK.
Yolanda CalleDepartment of Life Sciences, University of Roehampton, London, UK.
Claire M WellsSchool of Cancer and Pharmaceutical Sciences, New Hunts House, Kings College London, London, SE1 1UL, UK. Claire.wells@kcl.ac.uk.ORCID http://orcid.org/0000-0003-1926-6282
King's College London · GBUniversity of Roehampton · GBChinese University of Hong Kong · HK

Funding

Dr. Werner Jackstädt-Stiftung S 134 - 10113Pancreatic Cancer Research Fund _
6 · The paper itself

Abstract

backgroundMonocytes are a major component of the tumor microenvironment (TME) in pancreatic ductal adenocarcinoma (PDAC). However, the complex interactions between tumor cells and monocytes and their role in tumor invasion have not been fully established.

methodsTo specifically test the impact of interaction on invasive potential two PDAC cell lines PaTu8902 and CFPAC-1 were selected on their ability to form invasive adhesions, otherwise known as invadopodia and invade in a spheroid invasion assay.

resultsInterestingly when the PDAC cells were co-cultured with undifferentiated THP1 monocyte-like cells invadopodia formation was significantly suppressed. Moreover, conditioned media of THP1 cells (CM) was also able to suppress invadopodia formation. Further investigation revealed that both tissue inhibitor of metalloproteinase (TIMP) 1 and 2 were present in the CM. However, suppression of invadopodia formation was found that was specific to TIMP2 activity.

conclusionsOur findings indicate that TIMP2 levels in the tumour microenvironment may have prognostic value in patients with PDAC. Furthermore, activation of TIMP2 expressing monocytes in the primary tumour could present a potential therapeutic opportunity to suppress cell invasion in PDAC.

Indexed as

Carcinoma, Pancreatic DuctalCell CommunicationCell Line, TumorCell MovementCoculture TechniquesHumansMonocytesPancreatic NeoplasmsPodosomesSpheroids, CellularTHP-1 CellsTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2Tumor MicroenvironmentTIMP1 protein, humanTIMP2 protein, humanTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-2InvadopodiaMonocytesPancreatic ductal adenocarcinomaTIMP2Tumor microenvironment

Identifiers

PMID31836008
PMCPMC6911299
OpenAlexW2996059929

What OpenQuestion holds

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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.