Evidence map›Paper›PMID 32541644›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2020

LncRNA LINC00152 Increases the Aggressiveness of Human Retinoblastoma and Enhances Carboplatin and Adriamycin Resistance by Regulating MiR-613/Yes-Associated Protein 1 (YAP1) Axis.

Ying Wang, Danli Xin, Lei Zhou

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 29% 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, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. The Hippo signalling pathway and its impact on eye diseases.Journal of cellular and molecular medicine · 2024
    Pooled it
  2. Review
  3. Article
  4. Article
  5. The role of LncRNA-mediated autophagy in cancer progression.Frontiers in cell and developmental biology · 2024
    Review
  6. Article
  7. Review
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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

3 authors.

Ying WangDepartment of Ophthalmology, Ningbo Eye Hospital, Ningbo, Zhejiang, China (mainland).
Danli XinDepartment of Ophthalmology, Ningbo Eye Hospital, Ningbo, Zhejiang, China (mainland).
Lei ZhouDepartment of Ophthalmology, Ningbo Eye Hospital, Ningbo, Zhejiang, China (mainland).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Long noncoding RNA (lncRNA) acts as key regulator in human cancers, including retinoblastoma. However, the function of LINC00152 remains largely unknown in retinoblastoma. Thus, this study aimed to explore the role and molecular mechanisms of LINC00152 in retinoblastoma. MATERIAL AND METHODS The real-time quantitative polymerase chain reaction (RT-qPCR) was used to quantify the expression levels of LINC00152, miR-613 and yes-associated protein 1 (YAP1). The target genes of LINC00152 and miR-613 were identified by dual-luciferase reporter analysis, RNA immunoprecipitation (RIP) and RNA pulldown assays. The viability, apoptosis, and invasion of retinoblastoma cells were assessed by Cell Counting Kit-8, flow cytometry, and Transwell assays, respectively. In addition, western blot was used to test the protein expression in retinoblastoma cells or tissues. Cell sensitivity to carboplatin and adriamycin was analyzed by computing IC₅₀ value. The effects of LINC00152 silencing in vivo were measured by a xenograft experiment. RESULTS LINC00152 was obviously upregulated, while miR-613 was decreased in retinoblastoma tissues and cells. MiR-613, a target of LINC00152, was negatively regulated by LINC00152. Functional experiment further illustrated that silencing of LINC00152 evidently repressed proliferation, invasion, and autophagy while reinforced apoptosis of retinoblastoma cells, besides, retinoblastoma cells were more sensitive to carboplatin and adriamycin after knockdown of LINC00152. Importantly, knockdown of LINC00152-induced effects on retinoblastoma cells could be overturned by introducing miR-613 inhibitor. Downregulation of miR-613 abolished silencing of YAP1-effects on proliferation, apoptosis, invasion, autophagy, and chemoresistance of retinoblastoma cells. The results of the xenograft experiment indicated that LINC00152 silencing impeded tumor growth in vivo. CONCLUSIONS Mechanistically, LINC00152 enhanced the aggressiveness of retinoblastoma and boosted carboplatin and adriamycin resistance by regulating YAP1 by sponging miR-613 in human retinoblastoma.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntineoplastic AgentsApoptosisAutophagyCarboplatinCell Line, TumorCell ProliferationCell SurvivalChild, PreschoolDoxorubicinDrug Resistance, NeoplasmFemaleGene Knockdown TechniquesHumansInfantAdaptor Proteins, Signal TransducingAntineoplastic AgentsCarboplatinDoxorubicinlong non-coding RNA Linc00152, humanMicroRNAsMIRN613 microRNA, humanRNA, Long NoncodingRNA, MessengerTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID32541644
PMCPMC7315805
OpenAlexW3034657286

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.