Evidence map›Paper›PMID 32128112›Full record

ArticleCell & bioscience2020

A novel miR-0308-3p revealed by miRNA-seq of HBV-positive hepatocellular carcinoma suppresses cell proliferation and promotes G1/S arrest by targeting double CDK6/Cyclin D1 genes.

Xiaoming Dai, Ruixue Huang, Sai Hu, Yao Zhou, Xiaoya Sun, Pucheng Gui, Zijian Yu, Pingkun Zhou

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell & bioscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Xiaoming Dai *1The First Affiliated Hospital, University of South China, 69 Chuanshan Road, Hengyang, 421001 Hunan People's Republic of China.
Ruixue Huang *2Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078 China.
Sai Hu3Institute for Chemical Carcinogenesis, State Key Laboratory of Respiratory, Guangzhou Medical University, Guangzhou, 511436 People's Republic of China.
Yao Zhou2Department of Occupational and Environmental Health, Xiangya School of Public Health, Central South University, Changsha, 410078 China.
Xiaoya Sun3Institute for Chemical Carcinogenesis, State Key Laboratory of Respiratory, Guangzhou Medical University, Guangzhou, 511436 People's Republic of China.
Pucheng Gui1The First Affiliated Hospital, University of South China, 69 Chuanshan Road, Hengyang, 421001 Hunan People's Republic of China.
Zijian Yu1The First Affiliated Hospital, University of South China, 69 Chuanshan Road, Hengyang, 421001 Hunan People's Republic of China.
Pingkun Zhou3Institute for Chemical Carcinogenesis, State Key Laboratory of Respiratory, Guangzhou Medical University, Guangzhou, 511436 People's Republic of China.ORCID 0000-0002-5088-9608
First Affiliated Hospital of University of South China · CNCentral South University · CNState Key Laboratory of Respiratory Disease · CNBeijing Radiation Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPersistent infection with hepatitis B virus (HBV) accounts for the majority of hepatocellular carcinoma (HCC), but the molecular mechanisms underlying liver carcinogenesis are still not completely understood. Increasing evidence demonstrates that microRNAs (miRNAs) play significant functional roles in virus-host interactions. The aim of this study was to explore differentially expressed miRNA profiles and investigate the molecular mechanism of miR-0308-3p in HBV-positive HCC carcinogenesis.

methodsHigh-throughput sequencing was used to detect novel miRNAs in three samples of HBV-positive HCC tissue compared to matched HBV-negative HCC tissue. The Cancer Genome Atlas (TCGA) database was used to mine miRNAs related to HBV-positive HCC. Bioinformatics analyses were conducted to predict the miRNAs' possible biological and pathway regulatory functions. Quantitative polymerase chain reaction (qPCR) was then applied to evaluate the expression levels of randomly selected miRNAs. CCK-8 was used to measure cell proliferation and cell cycles were analyzed using flow cytometry. A dual luciferase reporter gene assay was used to confirm the downstream targets of miR-0308-3p.

resultsIn total, there were 34 overlapping miRNAs in both our miRNA-seq data and the TCGA database. We found two overlapping miRNAs in both the HBV-positive HCC samples and the TCGA database, and 205 novel pre-miRNA sequences were predicted. miR-522 and miR-523 were markedly overexpressed in HBV-positive HCC and were associated with a significantly poorer long-term prognosis (miR-522, HR 2.19, 95% CI 1.33-3.6,

conclusionsMiR-0308-3p upregulation dramatically suppressed HCC cell proliferation and induced G1/S cell cycle arrest by directly targeting CDK6/Cyclin D1. These findings reveal a novel molecular mechanism for activation of G1/S arrest in HCC and may prove clinically useful for developing new therapeutic targets.

Indexed as

CarcinogenesisHBVHCCmiRNA

Identifiers

PMID32128112
PMCPMC7047384
OpenAlexW3009530812

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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.