Evidence map›Paper›PMID 37248889›Full record

ArticleCancer biomarkers : section A of Disease markers2023

miR-383-5p serves as a tumor suppressor in bladder cancer by suppressing PI3K/AKT signaling pathway.

Yu Liu, Haitao Yu, Bin Zeng, Xin Gou, Ke Ren, Fangchao Yuan

Abstract read
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Article in Cancer biomarkers : section A of Disease markers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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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

5 citing papers in PubMed.

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4 · The record

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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.

Yu LiuDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Haitao YuDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Bin ZengDepartment of Breast and Thyroid Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xin GouDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ke RenDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Fangchao YuanDepartment of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs have been proven to be key molecules in human malignancy. However, to our knowledge, there is no study reporting miR-383-5p expression level and the role it plays in bladder cancer (BC).

methodsWe identified miR-383-5p to be one of the tumor-suppressing genes through using data from The Cancer Genome Atlas (TCGA) and GEO database. We evaluate the expression and activity of miR-383-5p in both BC tissue and cell lines. The impacts of miR-383-5p on proliferative, migratory ability and apoptotic rate in BC cell were evaluated by utilizing CCK-8 kits, flow cytometry, and Transwell assays. qRT-PCR, western blot, and luciferase reporter assays have been adopted to investigate the underlying mechanisms. In vivo tumorigenicity testing was conducted to determine the impact of miR-383-5p on BC cellular proliferative capacity.

resultsReduced miR-383-5p expression has been determined in BC tissue than in normal bladder tissue. Furthermore, BC cell proliferative, migratory ability was inhibited while apoptosis enhanced in vitro and in vivo by miR-383-5p up-regulation. In vitro and in vivo, silencing miR-383-5p considerably improved the growth and invasive capacity of cell, while decreased the apoptotic rates of BC cells.

conclusionmiR-383-5p plays its role as a tumor-suppressing gene by suppressing the PI3K/AKT signaling, hence preventing the development of BC.

Indexed as

MicroRNAsUrinary Bladder NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionMicroRNAsMIRN383 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKTbladder cancermiR-383-5pPI3KR1

Identifiers

PMID37248889
PMCPMC12412825

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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.