Evidence map›Paper›PMID 34904288›Full record

ArticleJournal of clinical laboratory analysis2022

Low-level EFCAB1 promoted progress by upregulated DNMT3B and could be as a potential biomarker in lung adenocarcinoma.

Xiang Yang, Wenjing Shi, Xiaolou Huang, Lijuan Hu, Junjun Wang, Fan Zhang, Yumin Wang, Kate Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
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  3. Comprehensive analysis of mFrontiers in immunology · 2022
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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

8 authors at 1 institution in 1 country.

Xiang YangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenjing ShiDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0003-3666-1110
Xiaolou HuangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Lijuan HuDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0002-6889-1650
Junjun WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0001-7038-2743
Fan ZhangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0002-7177-7218
Yumin WangDepartment of Laboratory Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0001-8243-3659
Kate HuangDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Wenzhou Medical University · CN

Funding

National Natural Science Foundation of China 81672088Wenzhou Municipal Science and Technology Bureau of China Y20190080Zhejiang Provincial Natural Science Foundation LY19H200002Zhejiang Provincial Research Center for Cancer Intelligent Diagnosis and Molecular Technology JBZX-202003
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) incidence is on the rise. We found that EFCAB1 (EF-Hand Calcium Binding Domain 1) was significantly downregulated in LUAD tissues, but the mechanism of EFCAB1 is unknown.

methodsOne hundred and two LUAD samples and corresponding NT samples were prospectively collected from patients at the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China, from August 2018 to August 2021.EFCAB1 expression was estimated in LUAD cells and tissues by qPCR. In-vitro cytology assays were used to detect the role of EFCAB1 in LUAD cells.

resultsEFCAB1 expression level of LUAD was significantly lower than it's adjacent cancer tissues and that of LUAD with big tumor size (>2 cm) was significantly lower than that of small tumor size (≤2 cm) group. It shown that expression levels of EFCAB1 from A549, HCC827, PC9 were lowly expressed. The cell migration, invasion, colony formation, proliferation ability of EFCAB1 OE A549, PC9 were lower than that of EFCAB1 OE A549, PC9 NC group, while the apoptotic cells percentage of the EFCAB1 OE A549, PC9 group were significantly increased. We found that DNMT1 mRNA expression level of PC9 was higher than that of BEAS-2B, while these of A549, HCC827 decreased. Compared with BEAS-2B, DNMT3A mRNA expression level of PC9 increased. DNMT3B mRNA expression level of PC9, HCC827 were higher than these of BEAS-2B.

conclusionThe EFCAB1 mRNA in LUAD patients and cell lines were downregulated; EFCAB1 overexpression inhibited cell proliferation, migration, invasion, while promoted apoptosis. EFCAB1 was expected to become a biomarker of LUAD.

Indexed as

Adenocarcinoma of LungDNA (Cytosine-5-)-MethyltransferasesLung NeoplasmsAdultAgedAged, 80 and overBiomarkersCalcium-Binding ProteinsCell MovementCell ProliferationCytoskeletal ProteinsDNA Methyltransferase 3BDown-RegulationFemaleHumansMaleBiomarkersCalcium-Binding ProteinsCLXN protein, humanCytoskeletal ProteinsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BRNA, MessengerbiomarkerEFCAB1lung adenocarcinomasmethylation

Identifiers

PMID34904288
PMCPMC8761460
OpenAlexW4200518590

What Socratic holds

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LicenceCC BY
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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 Socratic graph.