Evidence map›Paper›PMID 32606766›Full record

ArticleOncoTargets and therapy2020

MicroRNA-92a Targets SERTAD3 and Regulates the Growth, Invasion, and Migration of Prostate Cancer Cells via the P53 Pathway.

Shuo Zhang, Jia Yu, Bao-Fei Sun, Gui-Zhong Hou, Zi-Jiang Yu, Heng Luo

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. How MicroRNAs Command the Battle against Cancer.International journal of molecular sciences · 2024
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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 2 institutions in 1 country.

Shuo ZhangDepartment of Anatomy, School of Basic Medical Sciences, Guizhou Medical University, Guizhou, People's Republic of China.
Jia YuState Key Laboratory of Functions and Applications of Medicinal Plants, Guizhou Medical University, Guiyang, People's Republic of China.
Bao-Fei SunDepartment of Anatomy, School of Basic Medical Sciences, Guizhou Medical University, Guizhou, People's Republic of China.
Gui-Zhong HouDepartment of Anatomy, School of Basic Medical Sciences, Guizhou Medical University, Guizhou, People's Republic of China.
Zi-Jiang YuDepartment of Anatomy, School of Basic Medical Sciences, Guizhou Medical University, Guizhou, People's Republic of China.
Heng LuoDepartment of Anatomy, School of Basic Medical Sciences, Guizhou Medical University, Guizhou, People's Republic of China.
Affiliated Hospital of Guizhou Medical University · CNGuiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe miR-17-92 cluster, consisting of six mature miRNAs including miR-17, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a, plays a key role in the tumorigenesis and development of various cancers. The dysregulation of the cluster correlates with the biological mechanism of tumor growth and metastasis in vivo. However, the relationship between miR-17-92 cluster and malignancy of prostate cancer remains unclear, and its regulatory mechanism is worth investigating for controlling the proliferation and invasion of prostate cancer. MATERIALS AND

methodsThe expressions of miR-17-92 cluster members were measured using real-time quantitative RT-PCR. WB and real-time quantitative RT-PCR were used to detect the expression of SERTAD3, p38, p21, p53 protein levels and transcription levels. Cell proliferation and apoptosis were evaluated using cell proliferation assay, EdU and Hoechst assay, colony formation experiment and flow cytometry analyses. Cell migration and invasion were determined via transwell assays. The TargetScan, miRDB, starBase databases and luciferase reporter assays were used to confirm the target gene of miR-92a.

resultsThe relative expression of miR-92a was threefold higher in the metastatic PC-3 cells compared with the non-metastatic LNCaP cells. Down-regulation of miR-92a in PC-3 cells led to the inhibition of cell proliferation, migration, and invasion, while its overexpression in LNCaP cells resulted in the promotion of cell proliferation, migration, and invasion. The role of SERTAD3 in prostate cancer can be alleviated by miR-92a inhibitor.

conclusionSERTAD3 was the direct target gene of miR-92a in prostate cancer cells; inhibition of SERTAD3-dependent miR-92a alleviated the growth, invasion, and migration of prostate cancer cells by regulating the expression of the key genes of the p53 pathway, including p38, p53 and p21. These results suggested that targeting SERTAD3 by the induction of overexpression of miR-92a may be a treatment option in prostate cancer.

Indexed as

cell growthmetastasismiR-92aprostate cancerSERTAD3

Identifiers

PMID32606766
PMCPMC7298502
OpenAlexW3034346611

What OpenQuestion holds

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LicenceCC BY-NC
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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.