Evidence map›Paper›PMID 32581653›Full record

ArticleCancer cell international2020

Podoplanin is indispensable for cell motility and platelet-induced epithelial-to-mesenchymal transition-related gene expression in esophagus squamous carcinoma TE11A cells.

Nobuo Watanabe, Masako Kidokoro, Makiko Tanaka, Shigeaki Inoue, Tomoatsu Tsuji, Hisako Akatuska, Chisa Okada, Yumi Iida, Yoshinori Okada, Yusuke Suzuki and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.1field-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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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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

15 authors at 1 institution in 1 country.

Nobuo WatanabeDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.ORCID 0000-0002-2940-1604
Masako KidokoroDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Makiko TanakaDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Shigeaki InoueDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Tomoatsu TsujiDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Hisako AkatuskaDepartment of Host Defense Mechanism, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Chisa OkadaSupport Center for Medical Research and Education, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Yumi IidaSupport Center for Medical Research and Education, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Yoshinori OkadaSupport Center for Medical Research and Education, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Yusuke SuzukiSupport Center for Medical Research and Education, Tokai University, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Takehito SatoDepartment of Host Defense Mechanism, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Takashi YahataResearch Center for Regenerative Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Noriaki HirayamaInstitute of Advanced Biosciences, Tokai University, 411 Kitakaname, Hiratsuka, Kanagawa 259-1292 Japan.
Yoshihide NakagawaDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.
Sadaki InokuchiDepartment of Emergency and Critical Care Medicine, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193 Japan.ORCID 0000-0001-7320-2170
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe transmembrane glycoprotein podoplanin (PDPN) is upregulated in some tumors and has gained attention as a malignant tumor biomarker. PDPN molecules have platelet aggregation-stimulating domains and, are therefore, suggested to play a role in tumor-induced platelet activation, which in turn triggers epithelial-to-mesenchymal transition (EMT) and enhances the invasive and metastatic activities of tumor cells. In addition, as forced PDPN expression itself can alter the propensity of certain tumor cells in favor of EMT and enhance their invasive ability, it is also considered to be involved in the cell signaling system. Nevertheless, underlying mechanisms of PDPN in tumor cell invasive ability as well as EMT induction, especially by platelets, are still not fully understood.

methodsSubclonal TE11A cells were isolated from the human esophageal squamous carcinoma cell line TE11 and the effects of anti-PDPN neutralizing antibody as well as PDPN gene knockout on platelet-induced EMT-related gene expression were measured. Also, the effects of PDPN deficiency on cellular invasive ability and motility were assessed.

resultsPDPN-null cells were able to provoke platelet aggregation, suggesting that PDPN contribution to platelet activation in these cells is marginal. Nevertheless, expression of platelet-induced EMT-related genes, including vimentin, was impaired by PDPN-neutralizing antibody as well as PDPN deficiency, while their effects on TGF-β-induced gene expression were marginal. Unexpectedly, PDPN gene ablation, at least in either allele, engendered spontaneous N-cadherin upregulation and claudin-1 downregulation. Despite these seemingly EMT-like alterations, PDPN deficiency impaired cellular motility and invasive ability even after TGF-β-induced EMT induction.

conclusionsThese results suggested that, while PDPN seems to function in favor of maintaining the epithelial state of this cell line, it is indispensable for platelet-mediated induction of particular mesenchymal marker genes as well as the potentiation of motility and invasion capacity.

Indexed as

Crispr-Cas-9Esophageal squamous cell carcinomaKnockdownMetastasisPlatelet

Identifiers

PMID32581653
PMCPMC7310449
OpenAlexW3035993575

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.