Evidence map›Paper›PMID 37605406›Full record

ArticleCurrent pharmaceutical biotechnology2024

Anticancer Effect of Dihydroartemisinin

Jiaxin Yang, Tong Xia, Sijie Zhou, Sihao Liu, Tingyu Pan, Ying Li, Ziguo Luo

Abstract read
PubMed Publisher
In one paragraph

Article in Current pharmaceutical biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026
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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

7 authors at 1 institution in 1 country.

Jiaxin YangLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.ORCID 0000-0002-2048-2364
Tong XiaLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.
Sijie ZhouLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.
Sihao LiuLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.
Tingyu PanLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.
Ying LiLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.
Ziguo LuoLaboratory of Medical Experiment Technology, Institute of Life Science, Chongqing Medical University, Chongqing, China.ORCID 0009-0001-7353-1246
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDihydroartemisinin (DHA), a natural agent, exhibits potent anticancer activity. However, its biological activity on prostate cancer (PCa) 22Rv1 cells has not been previously investigated.

objectivesIn this study, we demonstrate that DHA induces anticancer effects through the induction of apoptosis and autophagy.

methodsCell viability and proliferation rate were assessed using the CCK-8 assay and cell clone formation assay. The generation of reactive oxygen species (ROS) was detected by flow cytometry. The molecular mechanism of DHA-induced apoptosis and autophagy was examined using Western blot and RT-qPCR. The formation of autophagosomes and the changes in autophagy flux were observed using transmission electron microscopy (TEM) and confocal microscopy. The effect of DHA combined with Chloroquine (CQ) was assessed using the EdU assay and flow cytometry. The expressions of ROS/AMPK/mTOR-related proteins were detected using Western blot. The interaction between Beclin-1 and Bcl-2 was examined using Co-IP.

resultsDHA inhibited 22Rv1 cell proliferation and induced apoptosis. DHA exerted its antiprostate cancer effects by increasing ROS levels. DHA promoted autophagy progression in 22Rv1 cells. Inhibition of autophagy enhanced the pro-apoptotic effect of DHA. DHA-induced autophagy initiation depended on the ROS/AMPK/mTOR pathway. After DHA treatment, the impact of Beclin- 1 on Bcl-2 was weakened, and its binding with Vps34 was enhanced.

conclusionDHA induces apoptosis and autophagy in 22Rv1 cells. The underlying mechanism may involve the regulation of ROS/AMPK/mTOR signaling pathways and the interaction between Beclin-1 and Bcl-2 proteins. Additionally, the combination of DHA and CQ may enhance the efficacy of DHA in inhibiting tumor cell activity.

Indexed as

ApoptosisArtemisininsAutophagyCell ProliferationProstatic NeoplasmsReactive Oxygen SpeciesAntineoplastic AgentsCell Line, TumorCell SurvivalHumansMaleTOR Serine-Threonine KinasesAntineoplastic AgentsArtemisininsartenimolReactive Oxygen SpeciesTOR Serine-Threonine Kinases22rv1.apoptosisautophagyDihydroartemisininmechanismprostate cancer

Identifiers

PMID37605406
OpenAlexW4386046701

What OpenQuestion holds

Textmetadata
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.