Evidence map›Paper›PMID 26343737›Full record

ArticleJournal of clinical medicine2015

MicroRNA-224 Induces G1/S Checkpoint Release in Liver Cancer.

Fangmei An, Alexandru V Olaru, Esteban Mezey, Qing Xie, Ling Li, Klaus B Piontek, Florin M Selaru

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. miR-224 Regulates the Aggressiveness of Hepatoma Cells Through the IL-6/STAT3/SMAD4 Pathway.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2021
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  13. MicroRNAs as paracrine signaling mediators in cancers and metabolic diseases.Best practice & research. Clinical endocrinology & metabolism · 2016
    Review
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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

7 authors at 3 institutions in 2 countries.

Fangmei AnDepartment of Gastroenterology, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, Jiangsu 214002, China. wdf8025@163.com.
Alexandru V OlaruDivision of Gastroenterology and Hepatology, Department of Medicine, The Johns Hopkins Hospital, Baltimore, MD, 21205, USA. aolaru1@jhmi.edu.
Esteban MezeyDivision of Gastroenterology and Hepatology, Department of Medicine, The Johns Hopkins Hospital, Baltimore, MD, 21205, USA. emezey@jhmi.edu.
Qing XieDepartment of Infectious Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. xieqingrjh@163.com.
Ling LiDivision of Gastroenterology and Hepatology, Department of Medicine, The Johns Hopkins Hospital, Baltimore, MD, 21205, USA. lli42@jhmi.edu.
Klaus B PiontekDivision of Gastroenterology and Hepatology, Department of Medicine, The Johns Hopkins Hospital, Baltimore, MD, 21205, USA. kpiontek@jhmi.edu.
Florin M SelaruDivision of Gastroenterology and Hepatology, Department of Medicine, The Johns Hopkins Hospital, Baltimore, MD, 21205, USA. fselaru1@jhmi.edu.
Johns Hopkins Hospital · USNanjing Medical University · CNShanghai Jiao Tong University · CN

Funding

MicroRNA involvement in the regulation of biliary epitheliumK08DK090154 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI SELARU, FLORIN · 2011 to 2015
$706k
NIDDK NIH HHS K08 DK090154
6 · The paper itself

Abstract

Profound changes in microRNA (miR) expression levels are frequently found in liver cancers compared to the normal liver. In this study, we evaluate the expression of miR-224 in human HCC and CCA, as well as its downstream targets and affected pathways. We show that miR-224 is upregulated in a large cohort of human CCA, similar to its upregulation in human HCC. For the purpose of studying the roles of miR-224 in HCC and CCA, we enforced miR-224 expression in cells. mRNA arrays followed by Ingenuity Pathway Analysis (IPA)-identified putative molecules and pathways downstream of miR-224. Phenotypically, we report that enforced expression of miR-224 increases the growth rate of normal cholangiocytes, CCA cell lines, and HCC cell lines. In addition, we identified, in an unbiased fashion, that one of the major biologic processes affected by miR-224 is Gap1 (G1) to Synthesis (S) transition checkpoint release. We next identified p21, p15, and CCNE1 as downstream targets of miR-224 and confirmed the coordinated downregulation results in the increased phosphorylation of Retinoblastoma (Rb) with resulting G1/S checkpoint release. Our data suggest that miR-224 is a master regulator of cell cycle progression, and that its overexpression results in G1/S checkpoint release followed by accelerated cell growth.

Indexed as

cell cyclecholangiocarcinomamiR-224

Identifiers

PMID26343737
PMCPMC4600154
OpenAlexW1917353195

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.