Evidence map›Paper›PMID 32240421›Full record

ArticleEsophagus : official journal of the Japan Esophageal Society2020

ATP6V0D2, a subunit associated with proton transport, serves an oncogenic role in esophagus cancer and is correlated with epithelial-mesenchymal transition.

Ming Qi, Dong-Mei Liu, Wei Ji, Hai-Ling Wang

Abstract read
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In one paragraph

Article in Esophagus : official journal of the Japan Esophageal Society, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

4 authors at 3 institutions in 1 country.

Ming QiDepartment of Digestive Medicine, Jinan City Central Hospital Affiliated to Shandong University, Jinan, 250013, Shandong, People's Republic of China.
Dong-Mei LiuEmergency Infusion Room, Jinan City Central Hospital Affiliated to Shandong University, Jinan, 250013, Shandong, People's Republic of China.
Wei JiClinical Experimental Research Center, Jinan City Central Hospital Affiliated to Shandong University, Jinan, 250013, Shandong, People's Republic of China.
Hai-Ling WangDepartment of Pharmacy, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, The East courtyard, No. 42 of West Culture Road, Lixia district, Jinan, 250014, Shandong, People's Republic of China. 13791077279@163.com.
Jinan Central Hospital · CNAffiliated Hospital of Shandong University of Traditional Chinese Medicine · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe poor prognosis of esophagus cancer (EC) is mainly due to its high invasiveness and metastasis, so it is urgent to search effectively prognostic markers and explore their roles in the mechanism of metastasis. MATERIALS AND

methodsBased on the TCGA database, we downloaded the RNA-Seq for analyzing the expression of ATP6V0D2. QRT-PCR was used to test the mRNA levels of ATP6V0D2 in cell lines. Chi-square tests were used to evaluate the correlation between ATP6V0D2 and clinical characteristics. Prognostic values were determined by Kaplan-Meier methods and cox's regression models. CCK-8 and clone formation assays were employed to evaluate the cell viability, and Transwell assay was implemented to determine the invasive and migratory abilities. Correlations between ATP6V0D2 and motion-related markers were analyzed by the GEPIA database and confirmed by western blot. Moreover, the relationship between ATP6V0D2 and molecules related to cell cycle and apoptosis was also determined by western blot.

resultsA significant increase was observed in 3 EC-related cell lines compared to the normal cell line. ATP6V0D2 has a connection with the poor prognosis and can be considered as an independent prognosticator for patients with EC. Besides, ATP6V0D2 can improve cells viability as well as invasive and migratory abilities. What's more, downregulation of ATP6V0D2 notably enhanced E-cadherin expression, while decreased N-cadherin, Vimentin, and MMP9 expression, whereas overexpression of ATP6V0D2 presented the opposite outcomes. Furthermore, we found that silencing ATP6V0D2 led to a significant reduction on the protein expression of Cyclin D1, CDK4, Bcl-2, whereas resulted in a notable enhancement on the Bax level.

conclusionATP6V0D2 might be an independent prognosticator for EC patients, and it possibly promotes tumorigenesis by regulating epithelial-mesenchymal transition, cell cycle and apoptosis-related markers, providing the possibility that ATP6V0D2 may be a novel biomarker for the therapeutic intervention of EC.

Indexed as

ApoptosisBiomarkers, TumorCadherinsCarcinogenesisCell CycleCell Line, TumorCell MovementCell SurvivalCyclin D1Cyclin-Dependent Kinase 4Epithelial-Mesenchymal TransitionEsophageal NeoplasmsFemaleGenes, bcl-2HumansMaleATP6V0D2 protein, humanBiomarkers, TumorCadherinsCCND1 protein, humanCDK4 protein, humanCyclin D1Cyclin-Dependent Kinase 4Matrix Metalloproteinase 9MMP9 protein, humanProtonsRNA, MessengerSincalideVacuolar Proton-Translocating ATPasesVimentinATP6V0D2InvasionMigrationPrognosisProliferation

Identifiers

PMID32240421
OpenAlexW3014424118

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.