Evidence map›Paper›PMID 26028032›Full record

ArticleOncogene2016

LPP inhibits collective cell migration during lung cancer dissemination.

S Kuriyama, M Yoshida, S Yano, N Aiba, T Kohno, Y Minamiya, A Goto, M Tanaka

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

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  18. Actin dynamics during tumor cell dissemination.International review of cell and molecular biology · 2021
    Review
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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

8 authors at 3 institutions in 1 country.

S KuriyamaDepartment of Molecular Medicine and Biochemistry, Graduate School and Faculty of Medicine, Akita University, Akita, Japan.
M YoshidaDepartment of Cellular and Organ pathology, Graduate School of and Faculty of Medicine, Akita University, Akita, Japan.
S YanoDivision of Medical Oncology, Cancer Therapeutics Development Program, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
N AibaDepartment of Molecular Medicine and Biochemistry, Graduate School and Faculty of Medicine, Akita University, Akita, Japan.
T KohnoDivision of Genome Biology, Group for Development of Molecular Diagnostics and Individualized Therapy, National Cancer Research Center Institute, Chiba, Japan.
Y MinamiyaDepartment of Thorasic Surgery, Akita University, Akita, Japan.
A GotoDepartment of Cellular and Organ pathology, Graduate School of and Faculty of Medicine, Akita University, Akita, Japan.
M TanakaDepartment of Molecular Medicine and Biochemistry, Graduate School and Faculty of Medicine, Akita University, Akita, Japan.
Akita University · JPChiba Cancer Center · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoma preferred partner (LPP) is a LIM domain protein, which has multiple functions as an actin-binding protein and a transcriptional coactivator, and it has been suggested that LPP has some roles in cell migration or invasion, however, its role in cancer cells remains to be elucidated. Here, we showed that LPP degraded N-cadherin in lung cancer, PC14PE6 cells via regulating the expression of matrix metalloproteinase 15 (MMP-15), and loss-of-LPP increases collective cell migration (CCM) and dissemination consequently. Knockdown of LPP and its functional partner, Etv5, markedly restores the full-length N-cadherin and increases cell-cell adhesion. We investigated the common target of LPP and Etv5, and found that MMP-15 is transcribed as their direct transcriptional target. Furthermore, MMP-15 could directly digest the N-cadherin extracellular domain. LPP knockdown in PC14PE6 cells increases N-cadherin-dependent CCM in the three-dimensional collagen gel invasion assays, and promoted the dissemination of cancer cells when they were orthotopically implanted in nude mice. Immunohistochemistry of lung adenocarcinoma specimens revealed the heterogeneity of LPP intensity and complementary expression of LPP and N-cadherin in the primary tumors. These findings suggest that loss-of-LPP, Etv5 or MMP-15 can be a prognostic marker of increasing malignancy.

Indexed as

Cell MovementNeoplasm MetastasisAdenocarcinomaAdenocarcinoma of LungAnimalsCadherinsCytoskeletal ProteinsDNA-Binding ProteinsFibroblastsGene Knockdown TechniquesHumansLIM Domain ProteinsLung NeoplasmsMaleMatrix Metalloproteinase 15MelanomaCadherinsCytoskeletal ProteinsDNA-Binding ProteinsETV5 protein, humanLIM Domain ProteinsLpp protein, mouseMatrix Metalloproteinase 15Transcription Factors

Identifiers

PMID26028032
OpenAlexW1599003087

What OpenQuestion holds

Textmetadata
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.