MicroRNA miR-182 cluster mediated modulation of RECK without changes in cell surface membrane type-1 matrix metalloproteinase (MT1-MMP).

Milagros Silva, Maria E Hernandez, Fausto Rojas, Lihua Li, Subbaya Subramanian, Michael J Wilson

Open access · greenAbstract read

In one paragraph

Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it

0cells of the map it votes in

3citing papers in PubMed

0.2field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025
Review
Effects of treadmill exercise on cerebral angiogenesis and MT1-MMP expression after cerebral ischemia in rats.Brain and behavior · 2018
Article
Peroxisome proliferator-activated receptor-γ agonist inhibits collagen synthesis in human keloid fibroblasts by suppression of early growth response-1 expression through upregulation of miR-543 expression.American journal of cancer research · 2016
Article

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

6 authors at 2 institutions in 1 country.

Milagros SilvaCentro de Investigaciones Cerebrales, Universidad Veracruzana Xalapa, Veracuz, MX ; Department of Laboratory Medicine and Pathology, University of Minnesota Minneapolis, MN, USA.

Maria E HernandezCentro de Investigaciones Cerebrales, Universidad Veracruzana Xalapa, Veracuz, MX ; Department of Laboratory Medicine and Pathology, University of Minnesota Minneapolis, MN, USA.

Fausto RojasCentro de Investigaciones Cerebrales, Universidad Veracruzana Xalapa, Veracuz, MX ; Department of Laboratory Medicine and Pathology, University of Minnesota Minneapolis, MN, USA.

Lihua LiDepartment of Surgery, University of Minnesota Minneapolis, MN, USA.

Subbaya SubramanianDepartment of Surgery, University of Minnesota Minneapolis, MN, USA ; Masonic Cancer Center, University of Minnesota Minneapolis, MN, USA.

Michael J WilsonDepartment of Laboratory Medicine and Pathology, University of Minnesota Minneapolis, MN, USA ; Masonic Cancer Center, University of Minnesota Minneapolis, MN, USA ; Department of Pharmacology, University of Minnesota Minneapolis, MN, USA ; Minneapolis VA Medical Center Minneapolis, MN, USA.

University of Minnesota · USUniversity of Minnesota System · US

Funding

Tumor Invasion and Metastasis Mediated by Cell Surface ProteolysisR01CA114418 · NCI · UNIVERSITY OF MINNESOTA · PI WILSON, MICHAEL J. · 2006 to 2010

$1.1M

NCI NIH HHS R01 CA114418

6 · The paper itself

Abstract

Cell surface localized membrane type 1-matrix metalloproteinase (MT1-MMP) plays an important role in physiological and pathological processes and its function can be regulated by proteins such as RECK. We examined the ability of miR-182 (one of the miR-183 cluster miRNAs), which can target RECK, to control cell surface MT1-MMP activity. Expression of RECK mRNA and protein was increased with anti-miRs to miR-182, miR-183 or miR-96 in HT1080 fibrosarcoma cells, but, decreased RECK mRNA and increased its protein in the benign prostatic hyperplasia cell line BPH-1. Treatment of BPH-1 and HT-1080 cells with the anti-miRs did not change the level of cell surface MT1-MMP activity, nor their rate of migration in an in vitro wound-healing assay. Trichostatin A (TSA) did not increase the level of RECK, but blocked cell surface MT1-MMP activity and decreased cell motility. Anti-miRs mediated increased RECK levels did not interfere with cell surface MT1-MMP function, and TSA may block cell surface localization of MT1-MMP by a mechanism independent of RECK.

Indexed as

EMMPRINmicroRNAmiR-182MT1-MMPRECKtrichostatin A (TSA)

Identifiers

PMID26609496

PMCPMC4633917

OpenAlexW2418283520

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.