Evidence map›Paper›PMID 28209205›Full record

ArticleJournal of hematology & oncology2017

Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer.

Fuzhen Qi, Xianghua Liu, Hao Wu, Xiang Yu, Chenchen Wei, Xiaodan Huang, Guozhong Ji, Fengqi Nie, Keming Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

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  6. Long Non-Coding RNAMolecules (Basel, Switzerland) · 2024
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23 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Fuzhen QiDepartment of Hepatopancreatobiliary Surgery, Huai'an First People's Hospital, Nanjing Medical University, Huai'an City, People's Republic of China.
Xianghua LiuDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People's Republic of China.
Hao WuDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Xiang YuDepartment of General Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, People's Republic of China.
Chenchen WeiDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Xiaodan HuangDepartment of Digestive Endoscopy and Medical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210011, People's Republic of China.
Guozhong JiDepartment of Digestive Endoscopy and Medical Center for Digestive Diseases, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210011, People's Republic of China. jigzefy@163.com.
Fengqi NieDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Keming WangDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
Second Affiliated Hospital of Nanjing Medical University · CNNanjing Medical University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong noncoding RNAs (lncRNAs) have emerged as important regulators of tumorigenesis and cancer progression. Recently, the lncRNA AGAP2-AS1 was identified as an oncogenic lncRNA in human non-small cell lung cancer (NSCLC) and its elevated expression was linked to NSCLC development and progression. However, the expression pattern and molecular mechanism of AGAP2-AS1 in gastric cancer (GC) have not been characterized.

methodsBioinformatic analysis was performed to determine AGAP2-AS1 expression levels in the GC and normal tissues using gene profiling data from the Gene Expression Omnibus. Quantitative real-time polymerase chain reaction was used to validate AGAP2-AS1 expression in the GC tissues/cell lines compared with that in the adjacent nontumorous tissues/normal epithelial cells. Loss- and gain-of-function approaches were performed to investigate the effect of AGAP2-AS1 on GC cell phenotypes. The effect of AGAP2-AS1 on cell proliferation was evaluated by MTT, colony formation, flow cytometry, and in vivo tumor formation assays. The effects of AGAP2-AS1 on cell migration and invasion were examined using Transwell assays. Chromatin immunoprecipitation, luciferase reporter assays, RNA pull-down, and RNA immunoprecipitation were used to investigate the factors involved in AGAP2-AS1 dysregulation and the mechanism of action of AGAP2-AS1 in the GC cells.

resultsAGAP2-AS1 was highly expressed in the GC tissues and cell lines, and patients with higher AGAP2-AS1 expression had a poorer prognosis and shorter overall survival. Furthermore, knockdown of AGAP2-AS1 significantly inhibited GC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. AGAP2-AS1 overexpression promoted cell growth and invasion. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription.

conclusionsTaken together, these findings imply that AGAP2-AS1 upregulated by SP1 plays an important role in GC development and progression by suppressing P21 and E-cadherin, which suggests that AGAP2-AS1 is a potential diagnostic marker and therapeutic target for GC patients.

Indexed as

BiopsyCadherinsCell Line, TumorCell ProliferationComputational BiologyCyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPrognosisRNA, Long NoncodingSp1 Transcription FactorStomach NeoplasmsTranscription, GeneticCadherinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21long non-coding RNA AGAP2-AS1, humanRNA, Long NoncodingSP1 protein, humanSp1 Transcription FactorAGAP2-AS1E-cadherinInvasionlncRNAMigrationP21Proliferation

Identifiers

PMID28209205
PMCPMC5314629
OpenAlexW2588995065

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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.