Evidence map›Paper›PMID 30679988›Full record

ArticleExperimental and therapeutic medicine2019

MicroRNA-361-3p regulates retinoblastoma cell proliferation and stemness by targeting hedgehog signaling.

Dan Zhao, Zhe Cui

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 53 citations in OpenAlex.

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  10. The functional role of circular RNAs in the pathogenesis of retinoblastoma: a new potential biomarker and therapeutic target?Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
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  19. Review
  20. Circular RNAMolecular therapy oncolytics · 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

2 authors at 1 institution in 1 country.

Dan ZhaoDepartment of Ophthalmology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161000, P.R. China.
Zhe CuiDepartment of Ophthalmology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161000, P.R. China.
Qiqihar Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoblastoma (RB) is the most common type of intraocular malignancy in children. During RB oncogenesis, sonic hedgehog (SHH) is commonly differentially expressed. Additionally, microRNAs (miRs) are known to serve crucial roles as oncogenes or tumor suppressors. Specifically, miR-361-3p has been revealed to serve a vital role in cutaneous squamous cell carcinoma, cervical cancer, prostate cancer, colorectal cancer, gastric cancer, hepatocellular carcinoma, breast cancer and lung cancer. However, the role of miR-361-3p in RB and the potential molecular mechanisms involved remain unknown. Therefore, the current study aimed to determine the involvement of miR-361-3p in the development of RB by targeting SHH signaling. In the present study, miR-361-3p expression levels in RB tissue and serum samples obtained from 10 patients with RB, normal retinal tissue and serum samples obtained from 10 healthy controls, and two human RB cell lines (Y79 and Weri-Rb-1) were determined using reverse transcription-quantitative polymerase chain reaction. In addition, a cell counting kit-8 assay, a cell transfection assay, a MTT assay, western blotting, a tumor sphere formation assay and a luciferase assay were used to assess the expression, function and molecular mechanism of miR-361-3p in human RB. It was demonstrated that miR-361-3p was significantly downregulated in RB tissues, RB serum and RB cell lines compared with normal retinal tissues and normal serum. The ectopic expression of miR-361-3p decreased RB cell proliferation and stemness. Furthermore, GLI1 and GLI3 were verified as potential direct targets of miR-361-3p. miR-361-3p was also revealed to exhibit a negative correlation with GLI1/3 expression in RB samples. Taken together, the results indicate that miR-361-3p functions as a tumor suppressor in the carcinogenesis and progression of RB by targeting SHH signaling. Thus, miR-361-3p should be further assessed as a potential therapeutic target for RB treatment.

Indexed as

glioma-associated oncogene homologue transcription factor 1glioma-associated oncogene homologue transcription factor 3hedgehog signalingmetastasismicroRNA-361-3pproliferationretinoblastoma

Identifiers

PMID30679988
PMCPMC6327618
OpenAlexW2902659550

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.