Evidence map›Paper›PMID 30030888›Full record

ArticleJournal of cellular and molecular medicine2018

LncRNA HOTAIR/miR-613/c-met axis modulated epithelial-mesenchymal transition of retinoblastoma cells.

Ge Yang, Yang Fu, Xiaoyan Lu, Menghua Wang, Hongtao Dong, Qiuming Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Long non-coding RNAs involved in retinoblastoma.Journal of cancer research and clinical oncology · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Progress of HOTAIR-microRNA in hepatocellular carcinoma.Hereditary cancer in clinical practice · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. LncRNA MBLN1-AS1 inhibits the progression of retinoblastoma through targeting miR-338-5p-Wnt/β-catenin signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  16. Article
  17. Article
  18. Article
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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.

Ge YangDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, China.
Yang FuDepartment of General Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, China.
Xiaoyan LuDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, China.
Menghua WangDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, China.
Hongtao DongDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, China.
Qiuming LiDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, China.ORCID 0000-0002-1983-9645
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since lncRNAs could modulate neoplastic development by modulating downstream miRNAs and genes, this study was carried out to figure out the synthetic contribution of HOTAIR, miR-613 and c-met to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumour-adjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXO-Rb44, SO-Rb50 and WERI-RB1) were also gathered. Moreover, transfections of pcDNA3.1-HOTAIR, si-HOTAIR, miR-613 mimic, miR-613 inhibitor, pcDNA3.1/c-met were performed to evaluate the influence of HOTAIR, miR-613 and c-met on viability, apoptosis and epithelial-mesenchymal transition (EMT) of retinoblastoma cells. Dual-luciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miR-613, as well as between miR-613 and c-met. Consequently, up-regulated HOTAIR and down-regulated miR-613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miR-613 elevated E-cadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also less-motivated (P < 0.05). Nonetheless, c-met prohibited the functioning of miR-613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miR-613, and c-met was the direct target gene of miR-613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miR-613/c-met signalling axis in modulating retinoblastoma cells' viability, apoptosis and expressions of EMT-specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.

Indexed as

ApoptosisCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMicroRNAsProto-Oncogene Proteins c-metRetinoblastomaRNA, Long NoncodingSignal TransductionSnail Family Transcription FactorsVimentinHOTAIR long untranslated RNA, humanMicroRNAsMIRN613 microRNA, humanProto-Oncogene Proteins c-metRNA, Long NoncodingSNAI1 protein, humanSnail Family Transcription FactorsVimentinc-metepithelial-mesenchymal transitionlncRNA HOTAIRmiR-613retinoblastoma

Identifiers

PMID30030888
PMCPMC6156449
OpenAlexW2883052116

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.