Evidence map›Paper›PMID 26190891›Full record

ArticleYonago acta medica2015

Anti-Proliferation Activity of Fucoidan in MKN45 Gastric Cancer Cells and Downregulation of Phosphorylated ASK1, a Cell Cycle-Regulated Kinase.

Miwa Yoshimoto, Katsumi Higaki, Eiji Nanba, Masahide Ikeguchi

Open access · greenAbstract read
In one paragraph

Article in Yonago acta medica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 25 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 1 institution in 1 country.

Miwa YoshimotoDivision of Surgical Oncology, Department of Surgery, School of Medicine, Tottori University Faculty of Medicine, Yonago 683-8504,Japan.
Katsumi Higaki†Division of Functional Genomics, Research Center for Bioscience and Technology, Tottori University, Yonago 683-8503,Japan.
Eiji Nanba†Division of Functional Genomics, Research Center for Bioscience and Technology, Tottori University, Yonago 683-8503,Japan.
Masahide IkeguchiDivision of Surgical Oncology, Department of Surgery, School of Medicine, Tottori University Faculty of Medicine, Yonago 683-8504,Japan.
Tottori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFucoidan is a high-molecular polysaccharide whose main constituent is sulfated fucose. We specifically focused on the anti-proliferation activity of fucoidan and examined the underlying mechanism in MKN45 gastric cancer cells.

methodsMKN45 cell proliferation was analyzed by BrdU assay and fucoidan cytotoxicity was examined by LDH and clonogenic assays. The Agilent Human microarray kit was used to identify upregulated and downregulated genes in response to fucoidan, and western blot analyses evaluated cell cycle proteins.

resultsFucoidan impeded the MKN45 cell cycle by approximately 50%, and inhibited cell proliferation.LDH assays showed no immediate cytotoxic effects of fucoidan at 24 h exposure, however longer time courses revealed cell growth inhibition at 4 days in a dose-dependent manner. Microarray analysis identified MAP3K5, or ASK1 (apoptosis signal-regulating kinase),which was upregulated by 1.38-fold upon fucoidan treatment.Fucoidan increased ASK1 protein levels, while reducing phosphorylated ASK1 levels. Reduction of ASK1 by siRNA decreased proliferation of MKN45 cells.

conclusionOur findings show that fucoidan may suppress cellular proliferation and DNA synthesis in MKN45 cells by suppressing the ASK1-p38 signaling pathway through reduction of phosphorylated ASK1 levels.

Indexed as

anti-proliferation activity;ASK1;cell cycle;fucoidan;MKN45

Identifiers

PMID26190891
PMCPMC4495266
OpenAlexW2160228678

What OpenQuestion holds

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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.