Evidence map›Paper›PMID 33387246›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2021

MicroRNA-596 is epigenetically inactivated and suppresses prostatic cancer cell growth and migration via regulating Wnt/β-catenin signaling.

J Dai, G Yuan, Y Li, H Zhou

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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 48% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
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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

4 authors at 1 institution in 1 country.

J DaiChongqing University Cancer Hospital, Chongqing, China.
G YuanChongqing University Cancer Hospital, Chongqing, China.
Y LiChongqing University Cancer Hospital, Chongqing, China.
H ZhouChongqing University Cancer Hospital, Chongqing, China. zhouhong1359@163.com.ORCID http://orcid.org/0000-0001-6615-1897
Chongqing University · CN

Funding

Key projects of Chongqing Health Commission 2016ZDXM031
6 · The paper itself

Abstract

objectivesAlthough studies have reported that miR-596 extensively participates in multiple cancer progression, the biological mechanisms and effects of miR-596 in prostatic cancer remain unclear. The literature is aimed to reveal the function and possible molecular mechanisms of miR-596 in prostatic cancer carcinogenesis. MATERIALS AND

methodsqRT-PCR was applied to examine miR-596 expression in prostatic cancer cell lines and samples, also methylation-specific PCR was used to detect the methylation status of the promoter CpG islands in prostatic cancer samples. Meanwhile, the tumor-related effects of miR-596 were detected via cell viability, clone formation assay, migration assay, flow cytometric and AO/EB assay. qRT-PCR and Western blots were applied to investigate the function of miR-596 on malignant behavior in prostatic cancer cells.

resultsWe found that miR-596 mRNA was decreased in prostatic cancer samples and cell lines. miR-596 mRNA level was also correlated to cancer stage, Gleason scores, while miR-596 promoter methylation was related to cancer tumor stage, Gleason score and preoperative PSA levels. miR-596 inhibited the cell growth and activity by causing cell apoptosis, and also suppressed the migration of prostatic cancer cells by revealing the epithelial-mesenchymal transition process. In addition, Western blot indicates that miR-596 overexpression deregulated Wnt/β-catenin signaling, by restraining phosphorylation levels of β-catenin and expression levels of downstream targets.

conclusionsIn summary, this research indicates that miR-596 overexpression could be potentially useful in the cell growth and migration of prostatic cancer and serves as a potential molecular marker in prostatic cancer.

Indexed as

Cell MovementCell ProliferationEpigenesis, GeneticHumansMaleMicroRNAsMiddle AgedProstatic NeoplasmsTumor Cells, CulturedMicroRNAsMIRN596 microRNA, humanMigrationmiR-596ProliferationProstatic cancerβ-catenin

Identifiers

PMID33387246
OpenAlexW3116140349

What OpenQuestion holds

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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.