Evidence map›Paper›PMID 24457988›Full record

ArticleCancer gene therapy2014

Critical role of miR-10b in transforming growth factor-β1-induced epithelial-mesenchymal transition in breast cancer.

Xu Han, Sun Yan, Zhang Weijie, Wang Feng, Wang Liuxing, Li Mengquan, Fan Qingxia

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

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  20. The Hippo pathway: an emerging role in urologic cancers.American journal of clinical and experimental urology · 2021
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5 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Xu HanDepartment of Breast Disease Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Sun YanDepartment of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Zhang WeijieDepartment of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Wang FengDepartment of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Wang LiuxingDepartment of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Li MengquanDepartment of Breast Disease Surgery, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Fan QingxiaDepartment of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
Zhengzhou University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a key process in the tumor metastatic cascade that is characterized by the loss of cell-cell junctions and cell polarity, resulting in the acquisition of migratory and invasive properties. Recent evidence showed that altered microRNA-10b (miR-10b) expression was implicated in the occurrence of EMT of breast cancer. However, the exact role and underlying mechanisms of miR-10b in the EMT of breast cancer still remain unknown. In this study, miR-10b was found to be upregulated in breast cancer tissues and breast cancer cell lines and the expression of miR-10b was shown to be closely correlated with aggressiveness in breast cancer. Treating breast cancer cells with the miR-10b inhibitor increased E-cadherin expression while decreasing vimentin expression. At the same time, on inhibition of miR-10b, the invasion and proliferation ability of breast cancer cells also decreased. Transforming growth factor-β (TGF-β) is a multifunctional cytokine that induces EMT in multiple cell types. Here, we identified miR-10b as a target gene of TGF-β1. The expression of miR-10b increased during TGF-β1-induced EMT of breast cancer cells. Further study showed that inhibition of miR-10b expression partially reversed the EMT, invasion and proliferation induced by TGF-β1 in breast cancer cells. Taken together, these results demonstrated a novel function for miR-10b in TGF-β1-induced EMT in breast cancer and increased their metastatic potential. MiR-10b might become a possible target for gene therapy in breast cancer.

Indexed as

Analysis of VarianceBlotting, WesternBreast NeoplasmsCadherinsCell Line, TumorCell ProliferationDNA, ComplementaryEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsNeoplasm InvasivenessReal-Time Polymerase Chain ReactionTransforming Growth Factor beta1VimentinCadherinsDNA, ComplementaryMicroRNAsMIRN10 microRNA, humanTGFB1 protein, humanTransforming Growth Factor beta1Vimentin

Identifiers

PMID24457988
OpenAlexW1994374023

What OpenQuestion holds

Textmetadata
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.