Evidence map›Paper›PMID 32322669›Full record

ArticleMolecular therapy oncolytics2020

Long Non-coding RNA EPIC1 Promotes Cell Proliferation and Motility and Drug Resistance in Glioma.

Jianjiao Wang, Shuguang Yang, Qiongyu Ji, Qingsong Li, Fenggang Zhou, Yang Li, Fei Yuan, Jie Liu, Yu Tian, Yan Zhao and 1 more

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

Article in Molecular therapy oncolytics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Association BetweenCancer control : journal of the Moffitt Cancer Center
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  14. Non-coding RNA in cancer.Essays in biochemistry · 2021
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  19. Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis.Frontiers in cell and developmental biology · 2021
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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 2 institutions in 1 country.

Jianjiao WangDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Shuguang YangHuxi Hospital Affiliated to Jining Medical College, Shanxian Central Hospital, Heze 274300, China.
Qiongyu JiDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Qingsong LiDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Fenggang ZhouDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yang LiDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Fei YuanDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Jie LiuDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yu TianDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yan ZhaoDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yongri ZhengDepartment of Neurosurgery, the 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Harbin Medical University · CNJining Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence has revealed that long non-coding RNAs (lncRNAs) are involved in carcinogenesis and tumor progression. lncRNAs play an important role in regulation of numerous cellular processes including cell proliferation, apoptosis, cell cycle, differentiation, and motility. Several studies have demonstrated that lncRNA EPIC1 governs cell growth, cell cycle, migration, invasion, and drug resistance in human malignancies. However, the role of EPIC1 and its underlying molecular mechanisms in glioma have not been investigated. In this study, we determined the function of EPIC1 in glioma cells via upregulation or downregulation of EPIC1. We further dissected the mechanism of EPIC1-mediated tumor progression in glioma. Our results showed that inhibition of EPIC1 suppressed cell viability, induced apoptosis, inhibited cell invasion, and increased cell sensitivity to temozolomide in glioma cells. Consistently, overexpression of EPIC1 exhibited the opposite effects in glioma cells. Moreover, our data suggest that EPIC1 exerts its biological functions via targeting Cdc20 in glioma cells. In line with this, overexpression of Cdc20 reversed the EPIC1-mediated tumor progression in glioma cells. Therefore, targeting EPIC1 might be a useful approach for glioma treatment.

Indexed as

cancerCdc20EPIC1gliomainvasionmigrationnon-coding RNAoncogeneproliferationtreatment

Identifiers

PMID32322669
PMCPMC7163045
OpenAlexW3015169977

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.