Evidence map›Paper›PMID 32931665›Full record

ArticleCancer medicine2020

The clinical value and potential molecular mechanism of the downregulation of MAOA in hepatocellular carcinoma tissues.

Yu-Yan Pang, Jian-Di Li, Li Gao, Xia Yang, Yi-Wu Dang, Ze-Feng Lai, Li-Min Liu, Jie Yang, Hua-Yu Wu, Rong-Quan He and 8 more

Abstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  20. Clinical Significance and Potential Role ofFrontiers in genetics · 2021
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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

18 authors.

Yu-Yan PangDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Jian-Di LiDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Li GaoDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Xia YangDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Yi-Wu DangDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Ze-Feng LaiSchool of Pharmacy, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Li-Min LiuSchool of Pharmacy, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Jie YangSchool of Pharmacy, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Hua-Yu WuDepartment of Cell Biology and Genetics, School of Pre-Clinical Medicine, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Rong-Quan HeDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Zhi-Guang HuangDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Dan-Dan XiongDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Li-Hua YangDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Lin ShiDepartment of Pathology, Second Affiliated Hospital of Guangxi Medical University, Nanning, P.R. China.
Wei-Jia MoDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Deng TangDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Hui-Ping LuDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.
Gang ChenDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, P.R. China.ORCID 0000-0003-2402-2987

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) remains one of the most common cancers worldwide and tends to be detected at an advanced stage. More effective biomarkers for HCC screening and prognosis assessment are needed and the mechanisms of HCC require further exploration. The role of MAOA in HCC has not been intensively investigated.

methodsIn-house tissue microarrays, genechips, and RNAsequencing datasets were integrated to explore the expression status and the clinical value of MAOA in HCC. Immunohistochemical staining was utilized to determine MAOA protein expression. Intersection genes of MAOA related co-expressed genes and differentially expressed genes were obtained to perform functional enrichment analyses. In vivo experiment was conducted to study the impact of traditional Chinese medicine nitidine chloride (NC) on MAOA in HCC.

resultsMAOA was downregulated and possessed an excellent discriminatory capability in HCC patients. Decreased MAOA correlated with poor prognosis in HCC patients. Downregulated MAOA protein was relevant to an advanced TNM stage in HCC patients. Co-expressed genes that positively related to MAOA were clustered in chemical carcinogenesis, where CYP2E1 was identified as the hub gene. In vivo experiment showed that nitidine chloride significantly upregulated MAOA in a nude mouse HCC model.

conclusionsA decreased MAOA level is not only correlated with aggressive behaviors in males but also serves as a promising biomarker for the diagnosis and prognosis of HCC patients. Moreover, MAOA may play a role in AFB1 toxic transformation through its synergistic action with co-expressed genes, especially CYP3A4. MAOA also serves as a potential therapy target of NC in HCC patients.

Indexed as

AnimalsAntineoplastic Agents, PhytogenicBenzophenanthridinesBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorCytochrome P-450 CYP2E1Cytochrome P-450 CYP3ADatabases, GeneticDown-RegulationGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansImmunohistochemistryLiver NeoplasmsAntineoplastic Agents, PhytogenicBenzophenanthridinesBiomarkers, TumorCYP3A4 protein, humanCytochrome P-450 CYP2E1Cytochrome P-450 CYP3AMonoamine Oxidasemonoamine oxidase A, humannitidinegene chipHCCimmunohistochemical stainingMAOARNA-seqtissue microarray

Identifiers

PMID32931665
PMCPMC7643659

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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.