Evidence map›Paper›PMID 30258911›Full record

ReviewGenes & diseases2017

Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor.

Daqing Wu

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & diseases, 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
–field-weighted citation impact, top 97% 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, 21 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

Daqing WuGeorgia Cancer Center and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Augusta University · US

Funding

Targeting chemoresistant prostate cancer with novel EED inhibitorsR01CA256058 · NCI · CLARK ATLANTA UNIVERSITY · PI DAQING WU · 2022 to 2026
$2.1M
EPLIN as a Molecular Target of Genistein in Preventing Prostate Cancer MetastasisR21CA164612 · NCI · EMORY UNIVERSITY · PI WU, DAQING · 2012 to 2013
$363k
Novel small-molecule targeted therapy for prostate cancerR41CA206725 · NCI · METCURE THERAPEUTICS, LLC · PI WU, DAQING · 2016 to 2016
$225k
Small-molecule therapy for metastatic prostate cancerR41CA217491 · NCI · METCURE THERAPEUTICS, LLC · PI WU, DAQING · 2017 to 2017
$225k
A Dietary Supplement As Adjunct Therapy In Castration-Resistant Prostate CancerR41CA186498 · NCI · METCURE THERAPEUTICS, LLC · PI WU, DAQING · 2015 to 2015
$161k
NCI NIH HHS R01 CA256058NCI NIH HHS R21 CA164612NCI NIH HHS R41 CA186498NCI NIH HHS R41 CA206725NCI NIH HHS R41 CA217491
6 · The paper itself

Abstract

The majority of cancer-related deaths are caused by tumor recurrence, metastasis and therapeutic resistance. During the late stages of tumor progression, multiple factors are involved, including the downregulation and/or loss of function of metastasis suppressors. Epithelial protein lost in neoplasm (EPLIN), an actin-binding protein, was initially identified as a putative tumor suppressor that is frequently downregulated in epithelial tumors. Recent evidence indicates that EPLIN may negatively regulate epithelia-to-mesenchymal transition (EMT), a crucial process by which cancer cells acquire invasive capabilities and therapeutic resistance. Importantly, downregulation of EPLIN is associated with clinical metastasis in a variety of solid tumors, suggesting that EPLIN could be a suppressor of metastasis. In this review, I will discuss the regulation and function of EPLIN in human cancer cells and explore the clinical significance of EPLIN in metastatic disease.

Indexed as

Actin cytoskeletonChemoresistanceEpithelial-to-mesenchymal transitionEPLINMetastasis suppressorTumor suppressor

Identifiers

PMID30258911
PMCPMC6136588
OpenAlexW2600514886

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.