Evidence map›Paper›PMID 27270442›Full record

ArticleOncogene2016

MicroRNA-101 regulated transcriptional modulator SUB1 plays a role in prostate cancer.

B V S K Chakravarthi, M T Goswami, S S Pathi, A D Robinson, M Cieślik, D S Chandrashekar, S Agarwal, J Siddiqui, S Daignault, S L Carskadon and 5 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  14. The Catalytic Subunit ofInternational journal of molecular sciences · 2022
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  18. PGC1α suppresses kidney cancer progression by inhibiting collagen-induced SNAIL expression.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Article
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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

15 authors at 4 institutions in 1 country.

B V S K ChakravarthiMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
M T GoswamiMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
S S PathiMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
A D RobinsonMolecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
M CieślikMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
D S ChandrashekarMolecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
S AgarwalMolecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
J SiddiquiMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
S DaignaultCenter for Cancer Biostatistics, Department of Biostatistics, University of Michigan, Ann Arbor, MI, USA.
S L CarskadonMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
X JingMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
A M ChinnaiyanMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
L P KunjuMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
N PalanisamyMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
S VaramballyMichigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · USMichigan Center for Translational Pathology · USUniversity of Alabama at Birmingham · USHoward Hughes Medical Institute · US

Funding

Regulation of Polycomb Repressive Complex 1 by EZH2 Regulated microRNAs in CancerR01CA157845 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI VARAMBALLY, SOORYANARAYANA · 2011 to 2015
$1.6M
Role of Transcriptional Corepressor CtBP1 in Prostate Cancer ProgressionR01CA154980 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI VARAMBALLY, SOORYANARAYANA · 2012 to 2016
$1.5M
NCI NIH HHS R01 CA154980NCI NIH HHS R01 CA157845
6 · The paper itself

Abstract

MicroRNA-101, a tumor suppressor microRNA (miR), is often downregulated in cancer and is known to target multiple oncogenes. Some of the genes that are negatively regulated by miR-101 expression include histone methyltransferase EZH2 (enhancer of zeste homolog 2), COX2 (cyclooxygenase-2), POMP (proteasome maturation protein), CERS6, STMN1, MCL-1 and ROCK2, among others. In the present study, we show that miR-101 targets transcriptional coactivator SUB1 homolog (Saccharomyces cerevisiae)/PC4 (positive cofactor 4) and regulates its expression. SUB1 is known to have diverse role in vital cell processes such as DNA replication, repair and heterochromatinization. SUB1 is known to modulate transcription and acts as a mediator between the upstream activators and general transcription machinery. Expression profiling in several cancers revealed SUB1 overexpression, suggesting a potential role in tumorigenesis. However, detailed regulation and function of SUB1 has not been elucidated. In this study, we show elevated expression of SUB1 in aggressive prostate cancer. Knockdown of SUB1 in prostate cancer cells resulted in reduced cell proliferation, invasion and migration in vitro, and tumor growth and metastasis in vivo. Gene expression analyses coupled with chromatin immunoprecipitation revealed that SUB1 binds to the promoter regions of several oncogenes such as PLK1 (Polo-like kinase 1), C-MYC, serine-threonine kinase BUB1B and regulates their expression. Additionally, we observed SUB1 downregulated CDKN1B expression. PLK1 knockdown or use of PLK1 inhibitor can mitigate oncogenic function of SUB1 in benign prostate cancer cells. Thus, our study suggests that miR-101 loss results in increased SUB1 expression and subsequent activation of known oncogenes driving prostate cancer progression and metastasis. This study therefore demonstrates functional role of SUB1 in prostate cancer, and identifies its regulation and potential downstream therapeutic targets of SUB1 in prostate cancer.

Indexed as

AnimalsCell ProliferationDNA-Binding ProteinsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansMaleMiceMicroRNAsProstatic NeoplasmsTranscription FactorsDNA-Binding ProteinsMicroRNAsMIRN101 microRNA, humanSUB1 protein, humanTranscription Factors

Identifiers

PMID27270442
PMCPMC5140777
OpenAlexW2414624742

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.