Evidence map›Paper›PMID 27765948›Full record

ArticleScientific reports2016

Suppression of iASPP-dependent aggressiveness in cervical cancer through reversal of methylation silencing of microRNA-124.

Peixin Dong, Ying Xiong, Hidemichi Watari, Sharon Jb Hanley, Yosuke Konno, Kei Ihira, Fumihiko Suzuki, Takahiro Yamada, Masataka Kudo, Junming Yue and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 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

11 authors at 4 institutions in 3 countries.

Peixin DongDepartment of Women's Health Educational System, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Ying XiongDepartment of Gynecology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, P. R. China.
Hidemichi WatariDepartment of Gynecology, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Sharon Jb HanleyDepartment of Women's Health Educational System, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Yosuke KonnoDepartment of Gynecology, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Kei IhiraDepartment of Gynecology, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Fumihiko SuzukiDepartment of Obstetrics and Gynecology, Tohoku University, Sendai 9808574, Japan.
Takahiro YamadaDepartment of Women's Health Educational System, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Masataka KudoDepartment of Gynecology, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Junming YueDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.
Noriaki SakuragiDepartment of Women's Health Educational System, Hokkaido University School of Medicine, Hokkaido University, N15, W7, Sapporo 0608638, Japan.
Hokkaido University · JPCenter for Cancer Research · USSun Yat-sen University Cancer Center · CNTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Derepression of wild-type p53 by suppressing its negative inhibitor iASPP (Inhibitor of apoptosis-stimulating protein of p53) represents a potential therapeutic option for cervical cancer (CC). Here, we reported a novel functional significance of iASPP upregulation in cervical tumorigenesis: iASPP acts as a key promoter of CC cell proliferation, epithelial-mesenchymal transition, invasion and cancer stemness, by interacting with p53 to suppress p53-mediated transcription of target genes and reducing p53-responsive microRNA-34a levels. Moreover, we demonstrate that miR-124, directly targeting iASPP, reduces expression of iASPP and attenuates CC cell growth and invasiveness. Low miR-124 expression is inversely correlated with increased expression of iASPP mRNA in CC tissues. In a cohort of 40 patients with CC, the low miR-124 expression was correlated with poor 5-year overall survival (P = 0.0002) and shorter disease-free survival 5-year (P = 0006). Treatment with the DNA methyltransferase inhibitor Zebularine increases miR-124 expression and retards CC cell growth and invasion with minimal toxicity to normal cells. Even at a non-toxic concentration, Zebularine was effective in suppressing CC cell invasion and migration. Altogether, the restoration of miR-124 reduces iASPP expression and leads to p53-dependent tumor suppression, suggesting a therapeutic strategy to treat iASPP-associated CC.

Indexed as

Gene SilencingBase SequenceCell Line, TumorCell ProliferationCytidineDNA MethylationEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMicroRNAsModels, BiologicalNeoplasm InvasivenessNeoplasm MetastasisNeoplastic Stem CellsCytidineIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN124 microRNA, humanPPP1R13L protein, humanpyrimidin-2-one beta-ribofuranosideRepressor ProteinsTumor Suppressor Protein p53

Identifiers

PMID27765948
PMCPMC5073231
OpenAlexW2533332734

What OpenQuestion holds

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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.