Evidence map›Paper›PMID 33968740›Full record

ArticleFrontiers in oncology2021

Downregulation of GLYAT Facilitates Tumor Growth and Metastasis and Poor Clinical Outcomes Through the PI3K/AKT/Snail Pathway in Human Breast Cancer.

Xin Tian, Lina Wu, Min Jiang, Zhenyong Zhang, Rong Wu, Jianing Miao, Caigang Liu, Song Gao

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  3. Evolutionary Transcriptomics of Cancer Development.International journal of molecular sciences · 2025
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  10. Accurate breast cancer diagnosis using a stable feature ranking algorithm.BMC medical informatics and decision making · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Xin TianDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Lina WuDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Min JiangDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Zhenyong ZhangDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Rong WuDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Jianing MiaoKey Laboratory of Shengjing Hospital, China Medical University, Shenyang, China.
Caigang LiuDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
Song GaoDepartment of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Glycine N-acyltransferase (GLYAT) gene encodes a protein that catalyzes the transfer of acyl groups from acyl CoA to glycine, resulting in acyl glycine and coenzyme A. Aberrant GLYAT expression is associated with several malignant tumors, but its clinical importance in human breast cancer (BC), has yet to be fully addressed. This study aims to evaluate the clinical function of GLYAT in BC patients.

methodsGLYAT expression was determined by immune blot and immunohistochemistry in three BC cell lines and primary cancer tissues. The MDA-MB 231 cell line was used for GLYAT gene knockdown experiments while the MCF7 cell line for overexpression experiments. Colony formation experiments, soft agar experiments, and transwell assays were utilized for further inspection of cell proliferation and migration capabilities. Immunofluorescence and western blot were used to detect markers of the epithelial-mesenchymal transition (EMT) and changes in the PI3K/AKT/Snail pathway. The role of GLYAT in tumor growth and metastasis was also assessed in nude mice

resultsGLYAT was decreased in human BC tissues and cell lines. Functional analysis showed that knockdown of GLYAT augmented BC cell proliferation

conclusionOur findings demonstrate that downregulation of GLYAT expression in human breast cancer is correlated with EMT

Indexed as

breast cancerclinicopathological featuresEMTGLYATPI3K/AKTprognosis

Identifiers

PMID33968740
PMCPMC8100313
OpenAlexW3112687303

What OpenQuestion holds

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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.