Evidence map›Paper›PMID 30843652›Full record

ArticleCancer medicine2019

Overexpression of long non-coding RNA NORAD promotes invasion and migration in malignant melanoma via regulating the MIR-205-EGLN2 pathway.

Yong Chen, Ke Cao, Jingjing Li, Aijun Wang, Lichun Sun, Jintian Tang, Wei Xiong, Xiao Zhou, Xiang Chen, Jianda Zhou and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-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

18 citing papers in PubMed, 42 citations in OpenAlex.

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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

11 authors at 6 institutions in 4 countries.

Yong ChenDepartment of Plastic Surgery of Third Xiangya Hospital, Changsha, China.
Ke CaoDepartment of Oncology of Third Xiangya Hospital, Changsha, China.
Jingjing LiDepartment of Plastic Surgery of Third Xiangya Hospital, Changsha, China.
Aijun WangSurgical Bioengineering Laboratory, Department of Surgery, UC Davis School of Medicine, Sacramento, California.
Lichun SunMedicine School of Tulane University Health Science Center, New Orleans, Louisiana.
Jintian TangInstitute of Medical Physics and Engineering, Department of Engineering Physics, Tsinghua University, Beijing, China.
Wei XiongCancer Research Institute, Key Laboratory of Carcinogenesis of Ministry of Health, Changsha, China.
Xiao ZhouDepartment of Head and Neck Surgery, Department of Oncology Plastic Surgery, Hunan Province Cancer Hospital, Changsha, China.
Xiang ChenDepartment of Dermatology of Xiangya Hospital, Changsha, China.
Jianda ZhouDepartment of Plastic Surgery of Third Xiangya Hospital, Changsha, China.ORCID 0000-0002-3766-6573
Yan LiuDepartment of Plastic Surgery of Third Xiangya Hospital, Changsha, China.
Central South University · CNHunan Cancer Hospital · CNMinistry of Education · SATsinghua University · CNTulane University · USUniversity of California Davis Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence suggests that long non-coding RNAs NORAD and miR-205 play a significant role in regulating cancer progression and metastasis. In this study, high expression of NORAD was firstly observed in melanoma tissues and human malignant melanoma cell lines, our aim was to study the interaction of them in the process of invasion and migration of malignant melanoma cells. NORAD, miR-205, and EGLN2 mRNA level in MM cells was detected by qRT-PCR. In situ hybridization (ISH) was performed to detect NORAD expression in MM tissues specimens. Effects of NORAD and miR-205 on Prolyl hydroxylase 2 (EGLN2) expression was explored by western blot in MM cells line. Dual-luciferase reporter assay was performed to verify the interaction relationship between NORAD and miR-205, as well as, miR-205 and EGLN2. Transwell assay was conducted to explore the effects of NORAD and miR-205 in vitro. Xenografts in nude mice experiment were used to confirm the role of NORAD and miR-205 in vivo. In vitro, NORAD knockdown significantly inhibited migration and invasion of malignant melanoma cells and elevated the expression of miR-205, there was an interaction between miR-205 and NORAD in the RNA-induced silencing complex. Upregulation of miR-205 induced significant inhibition of migratory and invasive ability compared with the scrambled control. However, downregulating NORAD largely reversed this effect. Furthermore, the regulatory effects of miR-205 on EGLN2 levels and the induction of endoplasmic reticulum stress were reversed by NORAD. In vivo, deletion of miR-205 induced tumor growth in nude mice. NORAD may play critical roles in tumorigenesis and progression of malignant melanoma by regulating of the miR-205-EGLN2 pathway, and may serve as a new therapeutic target.

Indexed as

AnimalsCell MovementCell ProliferationDown-RegulationEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansHypoxia-Inducible Factor-Proline DioxygenasesMaleMelanomaMice, NudeMicroRNAsNeoplasm InvasivenessNeoplasm TransplantationEGLN2 protein, humanHypoxia-Inducible Factor-Proline DioxygenasesMicroRNAsMIR205, humanNORAD long non-coding RNA, humanRNA, Long Noncodinglong non-coding RNAmelanomamicroRNAoncogene

Identifiers

PMID30843652
PMCPMC6488211
OpenAlexW2921849733

What OpenQuestion holds

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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.