Evidence map›Paper›PMID 20003467›Full record

ArticleJournal of experimental & clinical cancer research : CR2009

Lewis y antigen promotes the proliferation of ovarian carcinoma-derived RMG-I cells through the PI3K/Akt signaling pathway.

Juanjuan Liu, Bei Lin, Yingying Hao, Yue Qi, Liancheng Zhu, Feifei Li, Dawo Liu, Jianping Cong, Shulan Zhang, Masao Iwamori

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

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  18. Gene expression profile analysis in response to α1,2-fucosyl transferase (FUT1) gene transfection in epithelial ovarian carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

10 authors at 2 institutions in 2 countries.

Juanjuan LiuDepartment of Obstetrics and Gynecology, China Medical University Shengjing, Hospital, 36 Sanhao Street, Heping, Shenyang, 110004, PR China. juanjuanliu_lg@yahoo.com.cn
Bei Lin
Yingying Hao
Yue Qi
Liancheng Zhu
Feifei Li
Dawo Liu
Jianping Cong
Shulan Zhang
Masao Iwamori
China Medical University · CNKindai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLewis y antigen is difucosylated oligosaccharide and is carried by glycoconjugates at cell surface. Elevated expression of Lewis y has been found in 75% of ovarian tumor, and the high expression level is correlated to the tumor's pathological staging and prognosis. This study was to investigate the effect and the possible mechanism of Lewis y on the proliferation of human ovarian cancer cells.

methodsWe constructed a plasmid encoding alpha1,2-fucosyltransferase (alpha1,2-FT) gene and then transfected it into ovarian carcinoma-derived RMG-I cells with lowest Lewis y antigen expression level. Effect of Lewis y on cell proliferation was assessed after transfection. Changes in cell survival and signal transduction were evaluated after alpha-L-fucosidase, anti-Lewis y antibody and phosphatidylinositol 3-kinase (PI3K) inhibitor treatment.

resultsOur results showed that the levels of alpha1,2-FT gene and Lewis y increased significantly after transfection. The cell proliferation of ovarian carcinoma-derived RMG-I cells sped up as the Lewis y antigen was increased. Both of alpha-L-fucosidase and anti-Lewis y antibody inhibited the cell proliferation. The phosphorylation level of Akt was apparently elevated in Lewis y-overexpressing cells and the inhibitor of PI3K, LY294002, dramatically inhibited the growth of Lewis y-overexpressing cells. In addition, the phosphorylation intensity and difference in phosphorylation intensity between cells with different expression of alpha1,2-FT were attenuated significantly by the monoantibody to Lewis y and by the PI3K inhibitor LY294002.

conclusionsIncreased expression of Lewis y antigen plays an important role in promoting cell proliferation through activating PI3K/Akt signaling pathway in ovarian carcinoma-derived RMG-I cells. Inhibition of Lewis y expression may provide a new therapeutic approach for Lewis y positive ovarian cancer.

Indexed as

Blotting, WesternCell Line, TumorCell ProliferationEnzyme InhibitorsFemaleFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseHumansImmunohistochemistryLewis Blood Group AntigensOvarian NeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionSignal TransductionTransfectionEnzyme InhibitorsFucosyltransferasesGalactoside 2-alpha-L-fucosyltransferaseLewis Blood Group AntigensLewis Y antigenPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID20003467
PMCPMC2806302
OpenAlexW2106277152

What OpenQuestion holds

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LicenceCC BY
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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.