Evidence map›Paper›PMID 26650179›Full record

ArticleThe Journal of clinical investigation2016

Targeting ceramide synthase 6-dependent metastasis-prone phenotype in lung cancer cells.

Motoshi Suzuki, Ke Cao, Seiichi Kato, Yuji Komizu, Naoki Mizutani, Kouji Tanaka, Chinatsu Arima, Mei Chee Tai, Kiyoshi Yanagisawa, Norie Togawa and 20 more

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  4. Characterization of Lipid Alterations by OncogenicOmics : a journal of integrative biology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

30 authors at 8 institutions in 1 country.

Motoshi Suzuki
Ke Cao
Seiichi Kato
Yuji Komizu
Naoki Mizutani
Kouji Tanaka
Chinatsu Arima
Mei Chee Tai
Kiyoshi Yanagisawa
Norie Togawa
Takahiro Shiraishi
Noriyasu Usami
Tetsuo Taniguchi
Takayuki Fukui
Kohei Yokoi
Keiko Wakahara
Yoshinori Hasegawa
Yukiko Mizutani
Yasuyuki Igarashi
Jin-ichi Inokuchi
Soichiro Iwaki
Satoshi Fujii
Akira Satou
Yoko Matsumoto
Ryuichi Ueoka
Keiko Tamiya-Koizumi
Takashi Murate
Mitsuhiro Nakamura
Mamoru Kyogashima
Takashi Takahashi
Nagoya University · JPSojo University · JPHokkaido University · JPNagoya City University · JPNagoya University Hospital · JPGifu Pharmaceutical University · JPNihon Pharmaceutical University · JPTohoku Medical and Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingolipids make up a family of molecules associated with an array of biological functions, including cell death and migration. Sphingolipids are often altered in cancer, though how these alterations lead to tumor formation and progression is largely unknown. Here, we analyzed non-small-cell lung cancer (NSCLC) specimens and cell lines and determined that ceramide synthase 6 (CERS6) is markedly overexpressed compared with controls. Elevated CERS6 expression was due in part to reduction of microRNA-101 (miR-101) and was associated with increased invasion and poor prognosis. CERS6 knockdown in NSCLC cells altered the ceramide profile, resulting in decreased cell migration and invasion in vitro, and decreased the frequency of RAC1-positive lamellipodia formation while CERS6 overexpression promoted it. In murine models, CERS6 knockdown in transplanted NSCLC cells attenuated lung metastasis. Furthermore, combined treatment with l-α-dimyristoylphosphatidylcholine liposome and the glucosylceramide synthase inhibitor D-PDMP induced cell death in association with ceramide accumulation and promoted cancer cell apoptosis and tumor regression in murine models. Together, these results indicate that CERS6-dependent ceramide synthesis and maintenance of ceramide in the cellular membrane are essential for lamellipodia formation and metastasis. Moreover, these results suggest that targeting this homeostasis has potential as a therapeutic strategy for CERS6-overexpressing NSCLC.

Indexed as

AnimalsApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCeramidesDimyristoylphosphatidylcholineHumansLung NeoplasmsMaleMembrane ProteinsMiceMicroRNAsNeoplasm MetastasisPhenotypeSphingosine N-AcyltransferaseCeramidesCERS6 protein, humanDimyristoylphosphatidylcholineMembrane ProteinsMicroRNAsMIRN101 microRNA, humanSphingosine N-Acyltransferase

Identifiers

PMID26650179
PMCPMC4701566
OpenAlexW2191007858

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.