Evidence map›Paper›PMID 24448385›Full record

ArticleCancer biology & therapy2014

MicroRNA-148b and microRNA-152 reactivate tumor suppressor genes through suppression of DNA methyltransferase-1 gene in pancreatic cancer cell lines.

Masoumeh Azizi, Ladan Teimoori-Toolabi, Mohsen Karimi Arzanani, Kayhan Azadmanesh, Pezhman Fard-Esfahani, Sirous Zeinali

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In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 91 citations in OpenAlex.

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  15. Four-microRNA signature for detection of type 2 diabetes.World journal of clinical cases · 2020
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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

6 authors at 3 institutions in 2 countries.

Masoumeh AziziDepartment of Molecular Medicine; Biotechnology Research Center; Pasteur Institute of Iran; Tehran, Iran.
Ladan Teimoori-ToolabiDepartment of Molecular Medicine; Biotechnology Research Center; Pasteur Institute of Iran; Tehran, Iran.
Mohsen Karimi ArzananiCenter for Hematology and Regenerative Medicine; Karolinska Institute Huddinge; Stockholm, Sweden.
Kayhan AzadmaneshVirology Department; Pasteur Institute of Iran; Tehran, Iran.
Pezhman Fard-EsfahaniDepartment of Biochemistry; Pasteur Institute of Iran; Tehran, Iran.
Sirous ZeinaliDepartment of Molecular Medicine; Biotechnology Research Center; Pasteur Institute of Iran; Tehran, Iran.
Pasteur Institute of Iran · IRBiotechnology Research Center · IRKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of DNA methyltransferase 1 (DNMT-1) is observed mostly in pancreatic cancer and it can cause tumor suppressor genes silencing in this disease. Recent studies suggest that abnormal expressions of microRNAs (miRs) are involved in pathogenesis of different types of human cancers including pancreatic cancer. In this study we aimed to investigate the effect of miR-148b and -152 on reverting the tumorigenic phenotype of pancreatic cancer cell lines. In order to investigate whether miR-148b and -152 are involved in the regulation of DNMT-1, luciferase reporter assay was used and confirmed that the DNMT-1 mRNA could be a target for miR-148b and miR-152. Furthermore, overexpression of miR-148b and -152 in pancreatic cancer cell lines (MIA PaCa-2 and AsPC-1) decreased DNMT-1 expression (53% and 59% respectively), returned DNA methylation to normal patterns and induced re-expression of tumor suppressor genes, like BNIP3 (4.7- and 3.8-fold) and SPARC (5.3- and 2.9-fold) for miR-148b and -152 respectively. Moreover, the introduced miR-148b and -152 could inhibit the proliferation of MIA PaCa-2 (35% and 37% respectively) and AsPC-1 (39% and 40% respectively) cell lines. The apoptosis rates of MIA PaCa-1 after treatment with miR-148b and -152 were 10% and 8% respectively; while these rates in AsPC-1 were 16% and 11% respectively. Conclusively these findings mean that miRs that are targeting DNMT-1 and modifying methylation status of tumor suppressor genes such as BNIP3 and SPARC can be applied in killing the pancreatic cancer cells and decreasing the tumorigenicity of these cells.

Indexed as

ApoptosisCell Line, TumorCell ProliferationDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationGenes, Tumor SuppressorHumansMembrane ProteinsMicroRNAsOsteonectinPancreatic NeoplasmsProto-Oncogene ProteinsBNIP3 protein, humanDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNMT1 protein, humanMembrane ProteinsMicroRNAsMIRN148 microRNA, humanMIRN152 microRNA, humanOsteonectinProto-Oncogene ProteinsSPARC protein, humanDNMT1methylationmicroRNAspancreatic neoplasmstumor suppressor

Identifiers

PMID24448385
PMCPMC3979819
OpenAlexW2032741659

What OpenQuestion holds

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Registered trials

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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.