Evidence map›Paper›PMID 28526807›Full record

ArticleOncotarget2017

Dihydroartemisinin induces autophagy-dependent death in human tongue squamous cell carcinoma cells through DNA double-strand break-mediated oxidative stress.

Xinli Shi, Li Wang, Xiaoming Li, Jing Bai, Jianchun Li, Shenghao Li, Zeming Wang, Mingrui Zhou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.0field-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

19 citing papers in PubMed, 47 citations in OpenAlex.

  1. Correlation of signal transducer and activator of transcription-3 andThe Journal of international medical research · 2023
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  7. Terpenoids' anti-cancer effects: focus on autophagy.Apoptosis : an international journal on programmed cell death · 2021
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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

8 authors at 3 institutions in 1 country.

Xinli ShiDepartment of Otolaryngology Head and Neck Surgery, Bethune International Peace Hospital, Shijiazhuang 050081, China.
Li WangLaboratory of Organ Fibrosis Prophylaxis and Treatment by Combine Traditional Chinese and Western Medicine, Research Center of Combine Traditional Chinese and Western Medicine, Affiliated Traditional Medicine Hospital of Southwest Medical University, Luzhou 646000, China.
Xiaoming LiDepartment of Otolaryngology Head and Neck Surgery, Bethune International Peace Hospital, Shijiazhuang 050081, China.
Jing BaiDepartment of Otolaryngology Head and Neck Surgery, Bethune International Peace Hospital, Shijiazhuang 050081, China.
Jianchun LiLaboratory of Organ Fibrosis Prophylaxis and Treatment by Combine Traditional Chinese and Western Medicine, Research Center of Combine Traditional Chinese and Western Medicine, Affiliated Traditional Medicine Hospital of Southwest Medical University, Luzhou 646000, China.
Shenghao LiDepartment of Pathobiology and Immunology, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Zeming WangDepartment of Pathobiology and Immunology, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Mingrui ZhouDepartment of Pathobiology and Immunology, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.
Hebei University of Chinese Medicine · CNBethune International Peace Hospital · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dihydroartemisinin is an effective antimalarial agent with multiple biological activities. In the present investigation, we elucidated its therapeutic potential and working mechanism on human tongue squamous cell carcinoma (TSCC). It was demonstrated that dihydroartemisinin could significantly inhibit cell growth in a dose- and time-dependent manner by the Cell Counting Kit-8 and colony formation assay in vitro. Meanwhile, autophagy was promoted in the Cal-27 cells treated by dihydroartemisinin, evidenced by increased LC3B-II level, increased autophagosome formation, and increased Beclin-1 level compared to dihydroartemisinin-untreated cells. Importantly, dihydroartemisinin caused DNA double-strand break with simultaneously increased γH2AX foci and oxidative stress; this inhibited the nuclear localization of phosphorylated signal transducer and activator of transcription 3 (p-STAT3), finally leading to autophagic cell death. Furthermore, the antitumor effect of dihydroartemisinin-monotherapy was confirmed with a mouse xenograft model, and no kidney injury associated with toxic effect was observed after intraperitoneal injection with dihydroartemisinin for 3 weeks in vivo. In the present study, it was revealed that dihydroartemisinin-induced DNA double-strand break promoted oxidative stress, which decreased p-STAT3 (Tyr705) nuclear localization, and successively increased autophagic cell death in the Cal-27 cells. Thus, dihydroartemisinin alone may represent an effective and safe therapeutic agent for human TSCC.

Indexed as

AnimalsArtemisininsAutophagyCarcinoma, Squamous CellCell Line, TumorCell ProliferationDisease Models, AnimalDNA Breaks, Double-StrandedHumansModels, BiologicalOxidative StressSTAT3 Transcription FactorTongue NeoplasmsTumor BurdenXenograft Model Antitumor AssaysArtemisininsartenimolSTAT3 Transcription FactorautophagydihydroartemisininDNA double-strand breakhuman tongue squamous cell carcinomaSTAT3

Identifiers

PMID28526807
PMCPMC5542242
OpenAlexW2609425047

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.