Evidence map›Paper›PMID 23227138›Full record

ArticlePloS one2012

Akt mediates metastasis-associated gene 1 (MTA1) regulating the expression of E-cadherin and promoting the invasiveness of prostate cancer cells.

Hongyan Wang, Liangsheng Fan, Juncheng Wei, Yanjie Weng, Li Zhou, Ying Shi, Wenjuan Zhou, Ding Ma, Changyu Wang

RetractedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  13. MiR-106a promotes tumor growth, migration, and invasion by targetingAmerican journal of translational research · 2017
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  15. Diagnostic and prognostic values of tissue hsa-miR-30c and hsa-miR-203 in prostate carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Hongyan WangCancer Biology Research Center, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei, PR China.
Liangsheng Fan
Juncheng Wei
Yanjie Weng
Li Zhou
Ying Shi
Wenjuan Zhou
Ding Ma
Changyu Wang
Tongji Hospital · CNHuazhong University of Science and Technology · CNTianjin Central Hospital of Gynecology Obstetrics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human metastasis-associated gene 1 (MTA1) is highly associated with the metastasis of prostate cancer; however, the molecular functions of MTA1 that facilitate metastasis remain unclear. In this study, we demonstrate that the silencing of MTA1 by siRNA treatment results in the upregulation of E-cadherin expression by the phosphorylation of AKT (p-AKT) and decreases the invasiveness of prostate cancer cells. We show that MTA1 is expressed in over 90% of prostate cancer tissues, especially metastatic prostate cancer tissue, comparing to non-expression in normal prostate tissue. RT-PCR analysis and Western blot assay showed that MTA1 expression is significantly higher in highly metastatic prostate cancer PC-3M-1E8 cells (1E8) than in poorly metastatic prostate cancer PC-3M-2B4 cells (2B4). Silencing MTA1 expression by siRNA treatment in 1E8 cells increased the cellular malignant characters, including the cellular adhesive ability, decreased the cellular invasive ability and changed the polarity of cellular cytoskeleton. 1E8 cells over-expressing MTA1 had a reduced expression of E-cadherin, while 1E8 cells treated with MTA1 siRNA had a higher expression of E-cadherin. The expression of phosphorylated AKT (p-AKT) or the inhibition of p-AKT by wortmannin treatment (100 nM) significantly altered the function of MTA1 in the regulation of E-cadherin expression. Alterations in E-cadherin expression changed the role of p-AKT in cellular malignant characters. All of these results demonstrate that MTA1 plays an important role in controlling the malignant transformation of prostate cancer cells through the p-AKT/E-cadherin pathway. This study also provides a new mechanistic role for MTA1 in the regulation of prostate cancer metastasis.

Indexed as

Neoplasm InvasivenessBase SequenceCadherinsCell Line, TumorDNA PrimersGene SilencingHistone DeacetylasesHumansImmunohistochemistryMaleProstatic NeoplasmsProto-Oncogene Proteins c-aktReal-Time Polymerase Chain ReactionRepressor ProteinsTrans-ActivatorsCadherinsDNA PrimersHistone DeacetylasesMTA1 protein, humanProto-Oncogene Proteins c-aktRepressor ProteinsTrans-Activators

Identifiers

PMID23227138
PMCPMC3515600
OpenAlexW1976654954

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.