Evidence map›Paper›PMID 29543785›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Long Noncoding RNA Taurine-Upregulated Gene1 (TUG1) Promotes Tumor Growth and Metastasis Through TUG1/Mir-129-5p/Astrocyte-Elevated Gene-1 (AEG-1) Axis in Malignant Melanoma.

Jianwen Long, Qiqige Menggen, Qimige Wuren, Quan Shi, Xianming Pi

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  8. Interplay of LncRNA TUG1 and TGF-β/P53 Expression in Colorectal Cancer.Asian Pacific journal of cancer prevention : APJCP · 2023
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  18. Noncoding RNAs in apoptosis: identification and function.Turkish journal of biology = Turk biyoloji dergisi · 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

5 authors at 2 institutions in 1 country.

Jianwen LongDepartment of Dermatology, First Clinical Medicine School, Hubei University of Chinese Medicine, Wuhan, Hubei, China (mainland).
Qiqige MenggenDepartment of Dermatology, Mongolian Medicine Hospital of Bortala Mongolia Autonomous Prefecture, Bola, Bortala, China (mainland).
Qimige WurenDepartment of Dermatology, Mongolian Medicine Hospital of Bortala Mongolia Autonomous Prefecture, Bola, Bortala, China (mainland).
Quan ShiDepartment of Dermatology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei, China (mainland).
Xianming PiDepartment of Dermatology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, Hubei, China (mainland).
Hubei Provincial Hospital of Traditional Chinese Medicine · CNHubei University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Malignant melanoma is a class of malignant tumors derived from melanocytes. lncRNAs have been considered as pro-/anti-tumor factors in progression of cancers. The function of lncRNA TUG1 on growth of melanoma was investigated in this study. MATERIAL AND METHODS The TUG1 and miR-129-5p expression were examined via qRT-PCR. The protein expression was investigated by Western blotting assay. Luciferase reporter assay was used to assess if lncRNA TUG1 can bind to miR-129-5p and if miR-129-5p can target AEG1 mRNA. CCK-8 and apoptosis assay were used to detect cell growth and apoptosis. The metastasis of melanoma cells was detected by wound-healing and Transwell assays. The effects of TUG1 on growth of melanoma in vivo and cell chemoresistance were investigated via xenograft animal experiment and CCK-8 assay. RESULTS The expression of TUG1 and AEG1 was elevated and the miR-129-5p level was decreased in melanoma specimens and cell lines. Downregulation of either TUG1 or AEG1 suppressed cell growth and metastasis. miR-129-5p can bind directly to AEG1 and TUG1 can directly sponge miR-129-5p. Inhibition of TUG1 expression suppressed the expression of Bcl-2, MMP-9, and cyclin D1, and raised the level of cleaved caspase3 by modulating AEG1 level in melanoma cells. Inhibition of TUG1 reduced the growth of tumors in vivo and improved the chemosensitivity of A375 cells to cisplatin and 5-FU. CONCLUSIONS Reduction of TUG1 level suppressed cell growth and metastasis by regulating AEG1 expression mediated by targeting miR-129-5p. Suppression of lnc TUG1 may be a promising therapeutic strategy in the treatment of malignant melanoma.

Indexed as

Signal TransductionAdultAnimalsApoptosisBase SequenceCell Adhesion MoleculesCell Cycle CheckpointsCell Line, TumorCell ProliferationCutaneous Malignant MelanomaDown-RegulationFemaleGene Expression Regulation, NeoplasticGene SilencingHumansMaleCell Adhesion MoleculesMembrane ProteinsMicroRNAsMirn129 microRNA, humanMTDH protein, humanRNA-Binding ProteinsRNA, Long NoncodingTUG1 long noncoding RNA, human

Identifiers

PMID29543785
PMCPMC5866625
OpenAlexW2789453193

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.