Evidence map›Paper›PMID 29151917›Full record

ArticleOncology letters2017

Downregulation of lipolysis-stimulated lipoprotein receptor promotes cell invasion via claudin-1-mediated matrix metalloproteinases in human endometrial cancer.

Hiroshi Shimada, Seiro Satohisa, Takayuki Kohno, Takumi Konno, Ken-Ichi Takano, Syunta Takahashi, Tsubasa Hatakeyama, Chihiro Arimoto, Tsuyoshi Saito, Takashi Kojima

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-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

19 citing papers in PubMed, 25 citations in OpenAlex.

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  12. Leptin Downregulates Angulin-1 in Active Crohn's Disease via STAT3.International journal of molecular sciences · 2020
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  16. Structural Features of Tight-Junction Proteins.International journal of molecular sciences · 2019
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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

10 authors at 1 institution in 1 country.

Hiroshi ShimadaDepartment of Obstetrics and Gynecology, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Seiro SatohisaDepartment of Obstetrics and Gynecology, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Takayuki KohnoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Takumi KonnoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Ken-Ichi TakanoDepartment of Otolaryngology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido 060-8556, Japan.
Syunta TakahashiDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Tsubasa HatakeyamaDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Chihiro ArimotoDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Tsuyoshi SaitoDepartment of Obstetrics and Gynecology, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Takashi KojimaDepartment of Cell Science, Research Institute for Frontier Medicine, Sapporo, Hokkaido 060-8556, Japan.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipolysis-stimulated lipoprotein receptor (LSR) is a novel molecule present at tricellular contacts which recruits tricellulin (TRIC), a molecular component of tricellular tight junctions (tTJs). LSR and TRIC are colocalized with the bicellular tight junction (bTJ) protein claudin (CLDN)-1-based tight junction strands at tricellular corners. Knockdown of LSR in normal epithelial cells affects tTJ formation and the epithelial barrier function. In cancer cells knockdown of LSR has been demonstrated to increase cell invasion. However, the detailed mechanisms of how the downregulation of LSR enhances cell invasion in cancer remain unclear. In the present study, knockdown of LSR by small interfering RNA (siRNA) in Sawano human endometrial adenocarcinoma cells induced cell invasion. In LSR-knockdown Sawano cells, upregulation of CLDN-1 protein, which contributes to the cell invasion via matrix metalloproteinases (MMPs), was observed compared with the control group by western blotting and immunostaining. Knockdown of LSR significantly induced Sp1 transcription factor activity in the CLDN-1 promoter region. In LSR-knockdown Sawano cells, DNA microarray analysis demonstrated that MMP-1, MMP-2 and MMP-10 mRNA levels were increased, and the protein levels of membrane-type 1-MMP, MMP-2, MMP-9 and MMP-10 were shown to be increased on western blots. Knockdown of CLDN-1 with siRNA prevented the upregulation of cell invasion induced by the knockdown of LSR in Sawano cells. On the invasive front of human endometrial carcinoma tissue samples, a decrease in LSR and increase in CLDN-1 protein levels were observed using immunohistochemical methods. In conclusion, the results indicate that the downregulation of LSR promotes cell invasion of human endometrial cancer via CLDN-1 mediation of MMPs. This mechanism is important for studying the association of tTJs with the cellular invasion of cancer.

Indexed as

cell invasionclaudin-1endometrial cancerlipolysis-stimulated lipoprotein receptormatrix metalloproteinasesSp1 transcription factor

Identifiers

PMID29151917
PMCPMC5680700
OpenAlexW2756523589

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.