Evidence map›Paper›PMID 27588490›Full record

ReviewOncotarget2016

MicroRNAs and epithelial-mesenchymal transition in prostate cancer.

Kirandeep Sekhon, Nathan Bucay, Shahana Majid, Rajvir Dahiya, Sharanjot Saini

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.5field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Expression of microRNA-99a-3p in Prostate Cancer Based on Bioinformatics Data and Meta-Analysis of a Literature Review of 965 Cases.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Pooled it
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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

5 authors at 2 institutions in 1 country.

Kirandeep SekhonDepartment of Urology, Veterans Affairs Medical Center, San Francisco and University of California San Francisco, CA, USA.
Nathan BucayDepartment of Urology, Veterans Affairs Medical Center, San Francisco and University of California San Francisco, CA, USA.
Shahana MajidDepartment of Urology, Veterans Affairs Medical Center, San Francisco and University of California San Francisco, CA, USA.
Rajvir DahiyaDepartment of Urology, Veterans Affairs Medical Center, San Francisco and University of California San Francisco, CA, USA.
Sharanjot SainiDepartment of Urology, Veterans Affairs Medical Center, San Francisco and University of California San Francisco, CA, USA.
University of California, San Francisco · USSan Francisco VA Medical Center · US

Funding

MicroRNAs in the Progression and Metastisis of Prostate CancerR01CA138642 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAHIYA, RAJVIR · 2010 to 2014
$2.6M
MicroRNAs in frequently deleted loci regulate prostate cancer EMT and metastasisR01CA177984 · NCI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI SAINI, SHARANJOT · 2014 to 2018
$1.9M
NCI NIH HHS R01 CA138642NCI NIH HHS R01 CA177984
6 · The paper itself

Abstract

Prostate cancer (PCa) is a leading cause of male cancer-related deaths. A significant fraction of prostate tumors are very aggressive, often metastasizing to bone, causing significant morbidity and mortality. Also, PCa is associated with high rates of recurrence, often attributed to the existence of cancer stem cells. Epithelial-mesenchymal transition (EMT), a process characterized by decreased expression of epithelial genes and increased expression of mesenchymal genes, plays a critical role in tumor invasion, metastasis and recurrence. In PCa, EMT has been implicated particularly in the context of metastatic disease and microRNAs have emerged as critical post-transcriptional regulators of PCa EMT. In this review, we summarize the role of miRNAs in PCa EMT that play a role in progression, metastasis and recurrence. Studies till date suggest that microRNAs mediate efficient and reversible control of PCa EMT via multiple mechanisms including either by (i) directly repressing single or multiple EMT-TFs or regulating cytoskeletal components (epithelial/mesenchymal genes) or (ii) regulating key signaling pathways involved in EMT. Oncogenic microRNAs often act as EMT promoters by repressing epithelial characteristics and tumor suppressive miRNAs act by inhibiting mesenchymal progression. Further, EMT is mechanistically linked to stem cell signatures in PCa and several miRNAs implicated in EMT have been reported to influence PCa stem cells. Loss of EMT-inhibiting miRNAs and/or gain of EMT promoting miRNAs lead to induction of PCa EMT, leading to tumor progression, metastasis and recurrence. Restoring expression of tumor suppressive miRNAs and inhibiting oncogenic miRNAs represent potential therapeutic opportunities to prevent disease metastasis and recurrence.

Indexed as

MicroRNAsDisease ProgressionEpithelial-Mesenchymal TransitionHumansMaleNeoplasm InvasivenessNeoplasm Recurrence, LocalNeoplastic Stem CellsProstatic NeoplasmsMicroRNAsEMTmetastasismicroRNAsprostate cancerrecurrence

Identifiers

PMID27588490
PMCPMC5341899
OpenAlexW2509194659

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.