Evidence map›Paper›PMID 32902157›Full record

ArticleJournal of cellular and molecular medicine2020

CERS6 required for cell migration and metastasis in lung cancer.

Motoshi Suzuki, Ke Cao, Seiichi Kato, Naoki Mizutani, Kouji Tanaka, Chinatsu Arima, Mei Chee Tai, Norie Nakatani, Kiyoshi Yanagisawa, Toshiyuki Takeuchi and 17 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

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  14. MicroRNA 101 Attenuated NSCLC Proliferation through IDH2/HIFOxidative medicine and cellular longevity · 2022
    Article
  15. Article
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  17. CERS6 required for cell migration and metastasis in lung cancer.Journal of cellular and molecular medicine · 2020
    Article
  18. Review
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

27 authors at 6 institutions in 1 country.

Motoshi SuzukiDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID 0000-0003-0682-5006
Ke CaoDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Seiichi KatoDepartment of Pathology and Laboratory Medicine, Nagoya University Hospital, Nagoya, Japan.
Naoki MizutaniDepartment of Medical Technology, Nagoya University Graduate School of Health Sciences, Nagoya, Japan.
Kouji TanakaDepartment of Medical Technology, Nagoya University Graduate School of Health Sciences, Nagoya, Japan.
Chinatsu ArimaDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Mei Chee TaiDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Norie NakataniDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kiyoshi YanagisawaDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Toshiyuki TakeuchiDepartment of Molecular Oncology, Fujita Health University, Toyoake, Japan.
Hanxiao ShiDepartment of Molecular Oncology, Fujita Health University, Toyoake, Japan.
Yasuyoshi MizutaniDepartment of Molecular Oncology, Fujita Health University, Toyoake, Japan.
Atsuko NiimiDepartment of Molecular Oncology, Fujita Health University, Toyoake, Japan.
Tetsuo TaniguchiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Takayuki FukuiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kohei YokoiDepartment of Thoracic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keiko WakaharaDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yoshinori HasegawaDepartment of Respiratory Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yukiko MizutaniLaboratory of Biomembrane and Biofunctional Chemistry, Faculty of Advanced Life Science, Hokkaido University, Sapporo, Japan.
Soichiro IwakiDepartment of Molecular and Cellular Pathobiology and Therapeutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Satoshi FujiiDepartment of Molecular and Cellular Pathobiology and Therapeutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Akira SatouDepartment of Medical Technology, Nagoya University Graduate School of Health Sciences, Nagoya, Japan.
Keiko Tamiya-KoizumiDepartment of Molecular and Cellular Pathobiology and Therapeutics, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.
Takashi MurateDepartment of Medical Technology, Nagoya University Graduate School of Health Sciences, Nagoya, Japan.
Mamoru KyogashimaDivision of Microbiology and Molecular Cell Biology, Nihon Pharmaceutical University, Saitama, Japan.
Shuta TomidaDepartment of Biobank, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Takashi TakahashiDivision of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nagoya University · JPNagoya City University · JPFujita Health University · JPNagoya University Hospital · JPNihon Pharmaceutical University · JPOkayama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingolipids constitute a class of bio-reactive molecules that transmit signals and exhibit a variety of physical properties in various cell types, though their functions in cancer pathogenesis have yet to be elucidated. Analyses of gene expression profiles of clinical specimens and a panel of cell lines revealed that the ceramide synthase gene CERS6 was overexpressed in non-small-cell lung cancer (NSCLC) tissues, while elevated expression was shown to be associated with poor prognosis and lymph node metastasis. NSCLC profile and in vitro luciferase analysis results suggested that CERS6 overexpression is promoted, at least in part, by reduced miR-101 expression. Under a reduced CERS6 expression condition, the ceramide profile became altered, which was determined to be associated with decreased cell migration and invasion activities in vitro. Furthermore, CERS6 knockdown suppressed RAC1-positive lamellipodia/ruffling formation and attenuated lung metastasis efficiency in mice, while forced expression of CERS6 resulted in an opposite phenotype in examined cell lines. Based on these findings, we consider that ceramide synthesis by CERS6 has important roles in lung cancer migration and metastasis.

Indexed as

Cell MovementAnimalsBase SequenceCell Line, TumorCeramidesHumansLung NeoplasmsMaleMembrane ProteinsMice, NudeMicroRNAsModels, BiologicalNeoplasm MetastasisPseudopodiaSphingosine N-AcyltransferaseTreatment OutcomeCeramidesCERS6 protein, humanMembrane ProteinsMicroRNAsMIRN101 microRNA, humanSphingosine N-Acyltransferaseceramidelung cancermetastasismicro-RNA

Identifiers

PMID32902157
PMCPMC7579715
OpenAlexW3086257968

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.