Evidence map›Paper›PMID 26045994›Full record

ArticleAmerican journal of cancer research2015

miR-222/VGLL4/YAP-TEAD1 regulatory loop promotes proliferation and invasion of gastric cancer cells.

Nan Li, Nanrong Yu, Jia Wang, Haofeng Xi, Weiqun Lu, Houwei Xu, Min Deng, Guopei Zheng, Haiying Liu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  5. 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

9 authors at 1 institution in 1 country.

Nan LiDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Nanrong YuDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Jia WangDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Haofeng XiDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Weiqun LuDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Houwei XuDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Min DengDepartment of Cancer Research Institute of Affiliated Cancer Hospital of Guangzhou Medical University Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Guopei ZhengDepartment of Cancer Research Institute of Affiliated Cancer Hospital of Guangzhou Medical University Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Haiying LiuDepartment of Gastrointestinal Neoplasms Surgery Hengzhigang Road 78#, Guangzhou 510095, Guangdong, China.
Guangzhou Medical University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is one of the most common malignant tumors and recent data demonstrates the tumor suppressor role of VGLL4 in GC, but the mechanisms for VGLL4 downregulation in GC remain to be elucidated. Here, we confirmed the suppressor role of VGLL4 on proliferation and invasion in GC cells with over-activated YAP-TEAD signal, and indicated the reverse correlation between expression patters of VGLL4 and miR-222. Bioinformatics analysis combined with experimental confirmation revealed VGLL4 is a direct target of miR-222 in GC cells. Functionally, miR-222 inhibitor significantly inhibited GC cells proliferation and invasion and VGLL4 knockdown abolished the effects of miR-222 inhibitor. Moreover, TEAD1 knockdown resulted in decrease of miR-222 expression and increase of VGLL4 expression, and also resulted in reduction of luciferase activity driven by miR-222 promoter in GC cells, suggesting over-activated TEAD1 positively feedback transcriptionally regulates miR-222 expression via physically binding to the miR-222 promoter indicated by ChIP assay. Collectively, our findings implied the important role of miR-222/VGLL4/YAP-TEAD1 regulatory loop maintaining over-activated YAP-TEAD1 signal in GC cells, and enriched the rationale of VGLL4 in GC based on which a promising therapeutic strategy will be developed.

Indexed as

Gastric cancermiR-222TEAD1VGLL4

Identifiers

PMID26045994
PMCPMC4449443
OpenAlexW620440963

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.