Evidence map›Paper›PMID 27119499›Full record

ArticleOncotarget2016

Artemisinin and its derivatives can significantly inhibit lung tumorigenesis and tumor metastasis through Wnt/β-catenin signaling.

Yunli Tong, Yuting Liu, Hongming Zheng, Liang Zheng, Wenqin Liu, Jinjun Wu, Rilan Ou, Guiyu Zhang, Fangyuan Li, Ming Hu and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 117 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Yunli TongSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Yuting LiuSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Hongming ZhengInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Liang ZhengSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Wenqin LiuSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Jinjun WuInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Rilan OuInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Guiyu ZhangInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Fangyuan LiInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Ming HuInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Zhongqiu LiuSchool of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong, 510515, China.
Linlin LuInternational Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, China.
Guangzhou University of Chinese Medicine · CNSouthern Medical University · CNUniversity of Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small-cell lung cancer (NSCLC) is the most prevalent malignancy worldwide given its high incidence, considerable mortality, and poor prognosis. The anti-malaria compounds artemisinin (ART), dihydroartemisinin (DHA), and artesunate (ARTS) reportedly have anti-cancer potential, although the underlying mechanisms remain unclear. In this work, we used flow cytometry to show that ART, DHA, and ARTS could inhibit the proliferation of A549 and H1299 cells by arresting cell cycle in G1 phase. Meanwhile, tumor malignancy including migration, invasion, cancer stem cells, and epithelial-mesenchymal transition were also significantly suppressed by these compounds. Furthermore, ART, DHA, and ARTS remarkably decreased tumor growth in vivo. By using IWP-2, the inhibitor of Wnt/β-catenin pathway, and Wnt5a siRNA, we found that ART, DHA, and ARTS could render tumor inhibition partially dependent on Wnt/β-catenin inactivation. These compounds could strikingly decrease the protein level of Wnt5-a/b and simultaneously increase those of NKD2 and Axin2, ultimately resulting in β-catenin downregulation. In summary, our findings revealed that ART, DHA, and ARTS could suppress lung-tumor progression by inhibiting Wnt/β-catenin pathway, thereby suggesting a novel target for ART, DHA, and ARTS in cancer treatment.

Indexed as

A549 CellsAnimalsAntimalarialsArtemisininsArtesunatebeta CateninCarcinoma, Non-Small-Cell LungCell Cycle CheckpointsCell LineCell Line, TumorCell ProliferationCell Transformation, NeoplasticFemaleHumansLung NeoplasmsMice, Inbred BALB CAntimalarialsArtemisininsartenimolArtesunatebeta Cateninartemisininderivativenon-small-cell lung cancerWnt/β-catenin

Identifiers

PMID27119499
PMCPMC5058767
OpenAlexW2341415872

What OpenQuestion holds

Textmetadata
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.