Evidence map›Paper›PMID 32066878›Full record

ArticleOncogene2020

CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis.

Kai Liu, Ben-Jun Wang, WeiWei Han, Chun-Hua Chi, Chao Gu, Yu Wang, Xiaohai Fu, Wei Huang, Zhiguo Liu, Xilin Song

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  8. The Hippo signaling pathway in gastric cancer.Acta biochimica et biophysica Sinica · 2023
    Review
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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

10 authors at 4 institutions in 1 country.

Kai LiuDepartment of Gastrointestinal Surgery, Shandong Cancer Hospital and Institute, Jinan, China.
Ben-Jun WangDepartment of Anorectal Surgery, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.
WeiWei HanDepartment of Anorectal Surgery, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.
Chun-Hua ChiDepartment of Anorectal Surgery, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.
Chao GuDepartment of Anorectal Surgery, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.
Yu WangDepartment of Radiology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, 250014, China.
Xiaohai FuDepartment of Intensive Care Unit of Shouguang People's Hospital, Shouguang, Shandong, China.
Wei HuangDepartment of Radiation Oncology, Shandong Cancer Hospital and Institute, Jinan, China.
Zhiguo LiuPET-CT Center, Shandong Cancer Hospital and Institute, Jinan, China.
Xilin SongDepartment of Gastrointestinal Surgery, Shandong Cancer Hospital and Institute, Jinan, China. xilin_song1980@163.com.
Affiliated Hospital of Shandong University of Traditional Chinese Medicine · CNShandong First Medical University · CNShandong Tumor Hospital · CNShougang (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidences indicate that 3'UTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that acvr1b gene 3'UTR (acv3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of acv3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that acv3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in acv3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of acv3UTR. The positive correlation of acv3UTR and YAP1 expression, and the negative correlation of acv3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to acv3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of acv3UTR transcription in GC tumorigenesis, and indicates a correlation between 3'UTR trans-regulatory effect and GC development.

Indexed as

3' Untranslated RegionsActivin Receptors, Type IAdaptor Proteins, Signal TransducingAnimalsCarcinogenesisCell Line, TumorCell ProliferationCleavage And Polyadenylation Specificity FactorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMicroRNAsMiddle Aged3' Untranslated RegionsActivin Receptors, Type IACVR1B protein, humanAdaptor Proteins, Signal TransducingCleavage And Polyadenylation Specificity FactorMicroRNAsMIRN590 microRNA, humanNudt21 protein, humanRNA, Long NoncodingTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID32066878
PMCPMC7142022
OpenAlexW3041634142

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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.