Evidence map›Paper›PMID 24753748›Full record

ArticleInternational journal of clinical and experimental medicine2014

MiRNA-26b inhibits cellular proliferation by targeting CDK8 in breast cancer.

Jia Li, Xiaoyu Li, Xiangjie Kong, Qifeng Luo, Junfeng Zhang, Lin Fang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

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  18. Aberrant expression of CDK8 regulates the malignant phenotype and associated with poor prognosis in human laryngeal squamous cell carcinoma.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2017
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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 1 institution in 1 country.

Jia LiDepartment of Breast and Thyroid, Shanghai Tenth People's Hospital, College of Medicine, Tongji University Shanghai, China.
Xiaoyu LiDepartment of Breast and Thyroid, Shanghai Tenth People's Hospital, College of Medicine, Tongji University Shanghai, China.
Xiangjie KongDepartment of Breast and Thyroid, Shanghai Tenth People's Hospital, College of Medicine, Tongji University Shanghai, China.
Qifeng LuoDepartment of Breast and Thyroid, Shanghai Tenth People's Hospital, College of Medicine, Tongji University Shanghai, China.
Junfeng ZhangDepartment of Breast and Thyroid, Shanghai Tenth People's Hospital, College of Medicine, Tongji University Shanghai, China.
Lin FangDepartment of Breast and Thyroid, Shanghai Tenth People's Hospital, College of Medicine, Tongji University Shanghai, China.
Shanghai Tenth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMicroRNA-26b (miR-26b) has been reported to be down-regulated in a wide range of malignant tumors, However, the mechanism by which miR-26b is implicated in breast cancer tumorigenesis is incompletely understood. This study was undertaken to evaluate the expression pattern of miR-26b and characterize its biological role in human breast cancer.

methodsReverse transcription-polymerase chain reaction (RT-PCR) was used to quantify the expression levels of miR-26b in breast cancer and adjacent non-cancerous breast tissues. MTT, colony formation assay and cell cycle assay were carried out to characterize the miR-26b function. Finally, to validate the target gene of miR-26b, luciferase reporter assay was employed, followed by RT-PCR and Western blot confirmation.

resultsHere, we found that miR-26b expression was relatively downregulated in breast cancer specimens (P<0.01). Overexpression of miR-26b dramatically suppressed cell proliferation, colony formation and induced G0/G1 cell cycle arrest of MDA-MB-231 and Mcf-7 cells. Luciferase assays revealed that miR-26b directly targeted the 3'UTR of CDK8. Overexpression of miR-26b led to the downregulation of CDK8 and β-catenin expression. Similarly, CDK8 knockdown by siRNA suppressed cell growth and subsequent β-catenin expression.

conclusionsThese findings suggest that miR-26b exerts a tumor suppressive role in breast cancer and the miR-26b-mediated growth inhibition is achieved through suppression of a new target gene CDK8.

Indexed as

breast cancerCDK8cell cycleMiR-26bproliferation

Identifiers

PMID24753748
PMCPMC3992393
OpenAlexW1606452383

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.