Evidence map›Paper›PMID 30344920›Full record

ArticleOncotarget2018

The antiangiogenic action of cisplatin on endothelial cells is mediated through the release of tissue inhibitor of matrix metalloproteinases-1 from lung cancer cells.

Robert Ramer, Tilman Schmied, Christin Wagner, Maria Haustein, Burkhard Hinz

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  19. Tumor vessel normalization and immunotherapy in gastric cancer.Therapeutic advances in medical oncology · 2022
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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

5 authors at 1 institution in 1 country.

Robert RamerInstitute of Pharmacology and Toxicology, Rostock University Medical Center, Rostock, Germany.
Tilman SchmiedInstitute of Pharmacology and Toxicology, Rostock University Medical Center, Rostock, Germany.
Christin WagnerInstitute of Pharmacology and Toxicology, Rostock University Medical Center, Rostock, Germany.
Maria HausteinInstitute of Pharmacology and Toxicology, Rostock University Medical Center, Rostock, Germany.
Burkhard HinzInstitute of Pharmacology and Toxicology, Rostock University Medical Center, Rostock, Germany.
University of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to suppressing cancer cell proliferation and tumor growth, cisplatin has been shown to inhibit tumor angiogenesis. However, the underlying mechanism remains a matter of debate. The present study addressed the impact of cisplatin on potential tumor-to-endothelial cell communication conferring an antiangiogenic effect. For this purpose, migration and tube formation of human umbilical vein endothelial cells (HUVECs) exposed to conditioned media (CM) from vehicle- or cisplatin-treated A549 and H358 lung cancer cells were quantified. Cancer cells were exposed to non-toxic concentrations of cisplatin to mimic low-dose treatment conditions. CM from cancer cells exposed to cisplatin at concentrations of 0.01 to 1 µM elicited a concentration-dependent decrease in HUVEC migration and tube formation as compared with CM from vehicle-treated cells. The viability of HUVECs was virtually unaltered under these conditions. siRNA approaches revealed cisplatin-induced expression and subsequent release of tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) by lung cancer cells to be causally linked to a decrease in HUVEC migration and tube formation. Moreover, TIMP-1 upregulation and consequent inhibition of HUVEC migration by cisplatin was shown to be dependent on activation of p38 and p42/44 mitogen-activated protein kinases. Inhibition of angiogenic features was not observed when HUVECs were directly exposed to cisplatin. Similarly, antiangiogenic effects were not detectable in HUVECs exposed to CM from the cisplatin-challenged bronchial non-cancer cell line BEAS-2B. Collectively, the present data suggest a pivotal role of cisplatin-induced TIMP-1 release from lung cancer cells in tumor-to-endothelial cell communication resulting in a reduced cancer-associated angiogenic impact on endothelial cells.

Indexed as

cisplatinlow-dose metronomic treatmentlung cancer cellstissue inhibitor of matrix metalloproteinases-1tumor angiogenesis

Identifiers

PMID30344920
PMCPMC6183343
OpenAlexW2893750600

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.