Evidence map›Paper›PMID 32748357›Full record

ArticleEnvironmental science and pollution research international2020

SLC16A1-AS1 enhances radiosensitivity and represses cell proliferation and invasion by regulating the miR-301b-3p/CHD5 axis in hepatocellular carcinoma.

Shenglin Pei, Zuyi Chen, Huajun Tan, Liwei Fan, Baina Zhang, Chang Zhao

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Environmental science and pollution research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  9. Pan-Cancer Analysis Identifies CHD5 as a Potential Biomarker for Glioma.International journal of molecular sciences · 2022
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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 1 institution in 1 country.

Shenglin PeiDepartment of Anesthesiology, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, China.
Zuyi ChenDepartment of Intervention, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Qingxiu District, Nanning, 530021, Guangxi, China.
Huajun TanDepartment of Intervention, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Qingxiu District, Nanning, 530021, Guangxi, China.
Liwei FanDepartment of Intervention, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Qingxiu District, Nanning, 530021, Guangxi, China.
Baina ZhangDepartment of Intervention, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Qingxiu District, Nanning, 530021, Guangxi, China.
Chang ZhaoDepartment of Intervention, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Qingxiu District, Nanning, 530021, Guangxi, China. 710519137@qq.com.ORCID http://orcid.org/0000-0001-6413-8808
Tumor Hospital of Guangxi Medical University · CN

Funding

Key R & D plan of Guangxi Science and Technology Plan AB18221103
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), a common type of human malignancies, leads to increasing incidence and fairly high mortality. An increasing number of studies have verified that long noncoding RNAs (lncRNAs) played key roles in the development of multiple human cancers. As a biomarker, SLC16A1-AS1 has been reported in non-small cell lung cancer (NSCLC) and oral squamous cell carcinoma (OSCC). Thus, we decided to investigate whether SLC16A1-AS1 exerts its biological function in HCC. In this study, we discovered that SLC16A1-AS1 was obviously downregulated in HCC tissues and cells. Overexpression of SLC16A1-AS1 inhibited HCC cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) process as well as promoted cell apoptosis. Moreover, SLC16A1-AS1 was confirmed to enhance the radiosensitivity of HCC cells. Molecular mechanism exploration suggested that SLC16A1-AS1 served as a sponge for miR-301b-3p and CHD5 was the downstream target gene of miR-301b-3p in HCC cells. Rescue assays implied that CHD5 knockdown could recover the effects of SLC16A1-AS1 overexpression on HCC cellular processes. In brief, our study clarified that SLC16A1-AS1 acted as a tumor suppressor in HCC by targeting the miR-301b-3p/CHD5 axis, which may be a promising diagnostic biomarker and provide promising treatment for HCC patients.

Indexed as

Carcinoma, HepatocellularCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellLiver NeoplasmsLung NeoplasmsMicroRNAsMonocarboxylic Acid TransportersMouth NeoplasmsSymportersCell Line, TumorCell ProliferationDNA HelicasesGene Expression Regulation, NeoplasticHumansMonocarboxylate Transport Protein 1Nerve Tissue ProteinsCHD5 protein, humanDNA HelicasesMicroRNAsMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersNerve Tissue ProteinsSymportersCHD5Hepatocellular carcinomamiR-301b-3pRaidosensitivitySLC16A1-AS1

Identifiers

PMID32748357
OpenAlexW3047079259

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.