Evidence map›Paper›PMID 28332554›Full record

ArticleScientific reports2017

Fucoidan induces Toll-like receptor 4-regulated reactive oxygen species and promotes endoplasmic reticulum stress-mediated apoptosis in lung cancer.

Hsien-Yeh Hsu, Tung-Yi Lin, Mei-Kuang Lu, Pei-Ju Leng, Shu-Ming Tsao, Yu-Chung Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
18.4field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Article
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  19. Interaction of High-Molecular Weight Fucoidan fromInternational journal of molecular sciences · 2023
    Article
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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

6 authors at 4 institutions in 1 country.

Hsien-Yeh HsuDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Tung-Yi LinDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Mei-Kuang LuNational Research Institute of Chinese Medicine, Taipei, Taiwan.
Pei-Ju LengDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Shu-Ming TsaoDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Yu-Chung WuDivision of Thoracic Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWAcademia Sinica · TWNational Yang Ming Chiao Tung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fucoidan, a sulfated polysaccharide extracted from brown algae, exhibits anti-cancer activity. However, the effects and mechanism of fucoidan-induced apoptosis via endoplasmic reticulum (ER) stress is unclear. In this study, we demonstrated that fucoidan prevents tumorigenesis and reduces tumor size in LLC1-xenograft male C57BL/6 mice. Fucoidan induces an ER stress response by activating the PERK-ATF4-CHOP pathway, resulting in apoptotic cell death in vitro and in vivo. Furthermore, ATF4 knockdown abolishes fucoidan-induced CHOP expression and rescues cell viability. Specifically, fucoidan increases intracellular reactive oxygen species (ROS), which increase ATF4 and CHOP in lung cancer cells. Using the ROS scavenger N-acetyl-l-cysteine (NAC), we found that ROS generation is involved in fucoidan-induced ER stress-mediated apoptosis. Moreover, via Toll-like receptor 4 (TLR4) knockdown, we demonstrated that fucoidan-induced ROS and CHOP expression were attenuated. Our study is the first to identify a novel mechanism for the antitumor activity of fucoidan. We showed that fucoidan inhibits tumor viability by activating the TLR4/ROS/ER stress axis and the downstream PERK-ATF4-CHOP pathway, leading to apoptosis and suppression of lung cancer cell progression. Together, these results indicate that fucoidan is a potential preventive and therapeutic agent for lung cancer that acts via activation of ROS-dependent ER stress pathways.

Indexed as

Activating Transcription Factor 4AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticHumansLung NeoplasmsMicePhosphorylationPolysaccharidesProto-Oncogene Proteins c-aktActivating Transcription Factor 4Antineoplastic AgentsATF4 protein, humanfucoidanPolysaccharidesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesRNA, Small InterferingToll-Like Receptor 4Transcription Factor CHOP

Identifiers

PMID28332554
PMCPMC5362958
OpenAlexW2597927610

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.