Evidence map›Paper›PMID 32280078›Full record

ArticleCancer biomarkers : section A of Disease markers2020

Arsenic trioxide-induced upregulation of miR-1294 suppresses tumor growth in hepatocellular carcinoma by targeting TEAD1 and PIM1.

Xiaoniao Cai, Leilei Yu, Zhen Chen, Fangpeng Ye, Zonghai Ren, Peisheng Jin

Abstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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  11. Exploring the Mechanisms of Arsenic Trioxide (Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
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.

Xiaoniao CaiDepartment of Gastroenterology, Pingyang People's Hospital, Pingyang, Wenzhou, Zhejiang, China.
Leilei YuDepartment of Gastroenterology, Ruian People's Hospital, Ruian, Wenzhou, Zhejiang, China.
Zhen ChenDepartment of General Surgery, Ruian People's Hospital, Ruian, Wenzhou, Zhejiang, China.
Fangpeng YeDepartment of Gastroenterology, Ruian People's Hospital, Ruian, Wenzhou, Zhejiang, China.
Zonghai RenDepartment of Gastroenterology, Ruian People's Hospital, Ruian, Wenzhou, Zhejiang, China.
Peisheng JinDepartment of Gastroenterology, Ruian People's Hospital, Ruian, Wenzhou, Zhejiang, China.
Wenzhou Medical University · CNRuian People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, Arsenic trioxide (ATO) has been reported as an efficient drug for suppression of cancer cell growth. Existing studies revealed the extensive involvement of microRNAs (miRNAs) in initiation and development of hepatocellular carcinoma (HCC). However, the potential correlation between ATO and miRNAs in HCC progression remains to be explored. To conduct our research, we applied a qRT-PCR analysis to find miRNAs that were upregulated in HCC cells treated with ATO. In our present study, miR-1294 was found to be significantly upregulated in ATO-treated HCC cells. To confirm the function of ATO and miR-1294 in HCC progression, gain-of function assays were designed and conducted. As expected, proliferative ability of ATO-treated HCC cells was markedly weakened compared to DMSO-treated HCC cells. More importantly, proliferation was further suppressed in ATO-induced HCC cells after overexpression of miR-1294. Through bioinformatics analysis, some potential targets of miR-1294 were predicted. Further investigation revealed that Pim-1 proto-oncogene (PIM1) and TEA domain transcription factor 1 (TEAD1) were two downstream targets of miR-1294 and could be negatively regulated by ATO. Functionally, we determined that cell proliferation and apoptosis resistance suppressed by miR-1294 and ATO were recovered by introduction of TEAD1 and PIM1. Collectively, this study revealed that a novel ATO-miR-1294-TEAD1/PIM1 axis regulated HCC cell growth, offering a potential insight into the HCC therapy.

Indexed as

AnimalsApoptosisArsenic TrioxideCarcinoma, HepatocellularCell Line, TumorCell ProliferationComputational BiologyDNA-Binding ProteinsFemaleGain of Function MutationGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceMicroRNAsNuclear ProteinsArsenic TrioxideDNA-Binding ProteinsMAS1 protein, humanMicroRNAsMIRN1294 microRNA, humanNuclear ProteinsPIM1 protein, humanProto-Oncogene MasProto-Oncogene Proteins c-pim-1TEAD1 protein, humanTEA Domain Transcription FactorsTranscription FactorsATOhepatocellular carcinomamiR-1294PIM1TEAD1

Identifiers

PMID32280078
PMCPMC12662351
OpenAlexW3015350848

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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.