Evidence map›Paper›PMID 34002044›Full record

ArticleCancer gene therapy2022

LncRNA MAGI2-AS3 inhibits tumor progression and angiogenesis by regulating ACY1 via interacting with transcription factor HEY1 in clear cell renal cell carcinoma.

Guanbo Wang, Hai Li, Yi Hou

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2022. 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
2.0field-weighted citation impact, top 13% 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, 25 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

3 authors at 2 institutions in 1 country.

Guanbo WangDepartment of Urology, China-Japan Union Hospital of Jilin University, Changchun, People's Republic of China.
Hai LiDepartment of Urology, China-Japan Union Hospital of Jilin University, Changchun, People's Republic of China.
Yi HouDepartment of Urology, China-Japan Union Hospital of Jilin University, Changchun, People's Republic of China. hyi@jlu.edu.cn.ORCID http://orcid.org/0000-0002-3590-7716
Jilin University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clear cell renal cell carcinoma (ccRCC) represents the most common type of RCC in adults, characterized by hyper-vascularization and metastatic relapse. Surgical resection is the main treatment due to poor response of ccRCC to radio-and chemotherapy. However, the high complexity of tumor vasculature in ccRCC has thwarted effects to develop new therapeutic strategies for ccRCC. In this study, we identify the anti-angiogenic activity of MAGI2-AS3 in ccRCC. 86 paired samples of tumor tissues and adjacent no-tumor tissues were collected from ccRCC patients. Dual-luciferase reporter assay, RIP, and ChIP assays were employed to confirm interactions between MAGI2-AS3, transcription factor HEY1, and the ACY1 gene. In other studies, we assayed human ccRCC cells RLC-310 for their viability, migration and invasion using CCK-8 detection and transwell chamber systems. Angiogenesis was evaluated in the Matrigel-based human umbilical vein endothelial cell (HUVEC)-RLC-310 coculture model and immunohistochemical staining for vascular endothelial growth factor (VEGF) and CD31 in tumor tissues collected from a xenograft ccRCC mouse model. MAGI2-AS3 and ACY1 expression was downregulated in ccRCC tissues, and low expression of MAGI2-AS3 was associated with poor patient survival. Overexpression of MAGI2-AS3 could reduce ccRCC cell viability and migration, inhibit vessel-like tube formation of HUVECs in vitro, and repress tumor growth and angiogenesis in vivo. MAGI2-AS3 bound with HEY1 and reduced the HEY1 enrichment at the ACY1 promoter region, thus increasing ACY1 gene transcription. HEY1 knockdown or ACY1 overexpression that resisted MAGI2-AS3 knockdown was found in the in vivo and in vitro settings. The present study demonstrates that MAGI2-AS3 exerts tumor-suppressive, anti-angiogenic activities in ccRCC by modulating the HEY1/ACY1 pathway, thus lending support for conducting further investigations of anti-angiogenesis therapy for ccRCC.

Indexed as

AmidohydrolasesBasic Helix-Loop-Helix ProteinsCarcinoma, Renal CellCell Cycle ProteinsKidney NeoplasmsRNA, Long NoncodingAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGuanylate KinasesHumansMiceNeoplasm Recurrence, LocalNeovascularization, PathologicAdaptor Proteins, Signal TransducingAmidohydrolasesaminoacylase IBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsGuanylate KinasesHEY1 protein, humanMAGI2 protein, humanRNA, Long NoncodingTranscription FactorsVascular Endothelial Growth Factor A

Identifiers

PMID34002044
OpenAlexW3163650301

What OpenQuestion holds

Textmetadata
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.