Evidence map›Paper›PMID 31294899›Full record

ArticleMolecular oncology2019

Inhibition of miR-34a-5p can rescue disruption of the p53-DAPK axis to suppress progression of clear cell renal cell carcinoma.

Zhi-Fei Jing, Jian-Bin Bi, Zeliang Li, Xiankui Liu, Jun Li, Yuyan Zhu, Xiao-Tong Zhang, Zhe Zhang, Zhenhua Li, Chui-Ze Kong

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Autophagy Regulation by Crosstalk between miRNAs and Ubiquitination System.International journal of molecular sciences · 2021
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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

10 authors at 1 institution in 1 country.

Zhi-Fei JingDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Jian-Bin BiDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Zeliang LiDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Xiankui LiuDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Jun LiDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Yuyan ZhuDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Xiao-Tong ZhangDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Zhe ZhangDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Zhenhua LiDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.
Chui-Ze KongDepartment of Urology, First Hospital of China Medical University, Shenyang, Liaoning, China.ORCID 0000-0002-0875-2173
First Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DAPK, a transcriptional target of the p53 protein, has long been characterized as a tumor suppressor that acts as a negative regulator in multiple cellular processes. However, increasing studies have suggested that the role of DAPK may vary depending on cell type and cellular context. Thus far, the expression and function of DAPK in clear cell renal cell carcinoma (ccRCC) remain ambiguous. Since ccRCC behaves in an atypical way with respect to p53, whether the p53-DAPK axis functions normally in ccRCC is also an intriguing question. Here, tissue specimens from 61 ccRCC patients were examined for DAPK expression. Functional studies regarding apoptosis, growth, and migration were used to determine the role of DAPK in renal cancer cells. The validity of the p53-DAPK axis in ccRCC was also determined. Our study identified DAPK as a negative regulator of ccRCC, and its expression was reduced in certain subgroups. However, the p53-DAPK axis was disrupted due to upregulation of miR-34a-5p under stressed conditions. miR-34a-5p was identified as a novel repressor of DAPK acting downstream of p53. Inhibition of miR-34a-5p can correct the p53-DAPK axis disruption by upregulating DAPK protein and may have potential to be used as a therapeutic target to improve outcomes for ccRCC patients.

Indexed as

Signal TransductionAgedAnimalsCarcinoma, Renal CellCell Line, TumorDeath-Associated Protein KinasesDisease ProgressionDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMice, Inbred BALB CMicroRNAsMiddle AgedDAPK1 protein, humanDeath-Associated Protein KinasesMicroRNAsMIRN34a microRNA, mouseMIRN34 microRNA, humanTumor Suppressor Protein p53clear cell renal cell carcinomaDAPKmiR-34a-5pp53

Identifiers

PMID31294899
PMCPMC6763763
OpenAlexW2960541652

What OpenQuestion holds

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LicenceCC BY
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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.