Evidence map›Paper›PMID 31203308›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Formiminotransferase Cyclodeaminase Suppresses Hepatocellular Carcinoma by Modulating Cell Apoptosis, DNA Damage, and Phosphatidylinositol 3-Kinases (PI3K)/Akt Signaling Pathway.

Jiajia Chen, Zemian Chen, Zhentian Huang, Hongrong Yu, Yanbing Li, Wenhua Huang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 42 citations in OpenAlex.

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  12. The Effects of Naringenin on miRNA-mRNA Profiles in HepaRG Cells.International journal of molecular sciences · 2021
    Article
  13. Screening Hub Genes of Hepatocellular Carcinoma Based on Public Databases.Computational and mathematical methods in medicine · 2021
    Article
  14. Article
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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

6 authors at 3 institutions in 1 country.

Jiajia ChenNational Key Discipline of Human Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Zemian ChenDepartment of Medical Oncology, Affiliated Chaozhou Central Hospital, Southern Medical University, Chaozhou, Guangdong, China (mainland).
Zhentian HuangDepartment of General Surgery, Affiliated Chaozhou Central Hospital, Southern Medical University, Chaozhou, Guangdong, China (mainland).
Hongrong YuDepartment of Human Anatomy, School of Preclinical Medicine, Guangxi Medical University, Nanning, Guangxi, China (mainland).
Yanbing LiNational Key Discipline of Human Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Wenhua HuangNational Key Discipline of Human Anatomy, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Southern Medical University · CNChaozhou Central Hospital · CNGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Formiminotransferase cyclodeaminase (FTCD) is a candidate tumor suppressor gene in hepatocellular carcinoma (HCC). However, the mechanism for reduced expression of FTCD and its functional role in HCC remains unclear. In this study, we explored the biological functions of FTCD in HCC. MATERIAL AND METHODS The expression and clinical correlation of FTCD in HCC tissue were analyzed using TCGA (The Cancer Genome Atlas) and a cohort of 60 HCC patients. The MEXPRESS platform was accessed to identify the methylation level in promoter region FTCD. CCK-8 assay and flow cytometry analysis were used to explore the proliferation, cell apoptosis proportion, and DNA damage in HCC cells with FTCD overexpression. Western blot analysis was performed to identify the downstream target of FTCD. RESULTS FTCD is significantly downregulated in HCC tissues and cell lines. Low FTCD expression is correlated with a poor prognosis (P<0.001) and an aggressive tumor phenotype, including AFP levels (P=0.009), tumor size (P=0.013), vascular invasion (P=0.001), BCLC stage (P=0.024), and pTNM stage (P<0.001). Bioinformatics analysis indicated promoter hypermethylation can result in decreased expression of FTCD. FTCD overexpression suppressed cell proliferation by promoting DNA damage and inducing cell apoptosis in HCC cells. FTCD overexpression resulted in increased level of PTEN protein, but a decrease in PI3K, total Akt, and phosphorylated Akt protein in HCC cells, suggesting involvement of the PI3K/Akt pathway. CONCLUSIONS FTCD acts as a tumor suppressor gene in HCC pathogenesis and progression and is a candidate prognostic marker and a possible therapeutic target for this disease.

Indexed as

AgedAmmonia-LyasesApoptosisCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationChinaDNA DamageFemaleGene Expression Regulation, NeoplasticGlutamate FormimidoyltransferaseHep G2 CellsHumansLiver NeoplasmsMaleAmmonia-LyasesFTCD protein, humanGlutamate FormimidoyltransferaseMultifunctional EnzymesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID31203308
PMCPMC6592141
OpenAlexW2949707279

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.