Evidence map›Paper›PMID 28811522›Full record

ArticleScientific reports2017

The lichen secondary metabolite atranorin suppresses lung cancer cell motility and tumorigenesis.

Rui Zhou, Yi Yang, So-Yeon Park, Thanh Thi Nguyen, Young-Woo Seo, Kyung Hwa Lee, Jae Hyuk Lee, Kyung Keun Kim, Jae-Seoun Hur, Hangun Kim

Erratum issuedOpen 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. An erratum has been issued. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
10.8field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 89 citations in OpenAlex.

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  19. Hydroxide-Mediated SMolecules (Basel, Switzerland) · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 2 countries.

Rui ZhouCollege of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Sunchon, Republic of Korea.
Yi YangCollege of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Sunchon, Republic of Korea.
So-Yeon ParkCollege of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Sunchon, Republic of Korea.
Thanh Thi NguyenKorean Lichen Research Institute, Sunchon National University, Sunchon, Republic of Korea.
Young-Woo SeoKorea Basic Science Institute, Gwangju Center, Gwangju, Republic of Korea.
Kyung Hwa LeeDepartment of Pathology, Chonnam National University Medical School, Gwangju, Republic of Korea.
Jae Hyuk LeeDepartment of Pathology, Chonnam National University Medical School, Gwangju, Republic of Korea.
Kyung Keun KimMedical Research Center for Gene Regulation, Chonnam National University Medical School, Gwangju, Republic of Korea.
Jae-Seoun HurKorean Lichen Research Institute, Sunchon National University, Sunchon, Republic of Korea.
Hangun KimCollege of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Sunchon, Republic of Korea. hangunkim@sunchon.ac.kr.
Sunchon National University · KRChonnam National University Hospital · KRChonnam National University · KRKorea Basic Science Institute · KRThai Nguyen University · VN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lichens are symbiotic organisms that produce various secondary metabolites. Here, different lichen extracts were examined to identify secondary metabolites with anti-migratory activity against human lung cancer cells. Everniastrum vexans had the most potent inhibitory activity, and atranorin was identified as an active subcomponent of this extract. Atranorin suppressed β-catenin-mediated TOPFLASH activity by inhibiting the nuclear import of β-catenin and downregulating β-catenin/LEF and c-jun/AP-1 downstream target genes such as CD44, cyclin-D1 and c-myc. Atranorin decreased KAI1 C-terminal interacting tetraspanin (KITENIN)-mediated AP-1 activity and the activity of the KITENIN 3'-untranslated region. The nuclear distribution of the AP-1 transcriptional factor, including c-jun and c-fos, was suppressed in atranorin-treated cells, and atranorin inhibited the activity of Rho GTPases including Rac1, Cdc42, and RhoA, whereas it had no effect on epithelial-mesenchymal transition markers. STAT-luciferase activity and nuclear STAT levels were decreased, whereas total STAT levels were moderately reduced. The human cell motility and lung cancer RT² Profiler PCR Arrays identified additional atranorin target genes. Atranorin significantly inhibited tumorigenesis in vitro and in vivo. Taken together, our results indicated that E. vexans and its subcomponent atranorin may inhibit lung cancer cell motility and tumorigenesis by affecting AP-1, Wnt, and STAT signaling and suppressing RhoGTPase activity.

Indexed as

Secondary MetabolismAntineoplastic Agentsbeta CateninBiological ProductsCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansHydroxybenzoatesLichensLung NeoplasmsProto-Oncogene Proteins c-junrho GTP-Binding ProteinsSignal TransductionAntineoplastic Agentsatranorinbeta CateninBiological ProductsHydroxybenzoatesProto-Oncogene Proteins c-junrho GTP-Binding ProteinsTranscription Factor AP-1

Identifiers

PMID28811522
PMCPMC5557893
OpenAlexW2742658004

What OpenQuestion holds

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LicenceCC BY
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.