Evidence map›Paper›PMID 28498397›Full record

ArticleInternational journal of molecular medicine2017

Dihydroartemisinin inhibits the viability of cervical cancer cells by upregulating caveolin 1 and mitochondrial carrier homolog 2: Involvement of p53 activation and NAD(P)H:quinone oxidoreductase 1 downregulation.

Ting Zhang, Yuan Hu, Ting Wang, Peiling Cai

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Different Role of Caveolin-1 Gene in the Progression of Gynecological Tumors.Asian Pacific journal of cancer prevention : APJCP · 2019
    Review
  13. Potential applications of artemisinins in ocular diseases.International journal of ophthalmology · 2019
    Review
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

4 authors at 2 institutions in 1 country.

Ting ZhangDepartment of Medical Cell Biology and Genetics, Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Yuan HuDepartment of Anatomy and Histology, School of Medicine, Chengdu University, Chengdu, Sichuan 610106, P.R. China.
Ting WangDepartment of Anatomy and Histology, School of Medicine, Chengdu University, Chengdu, Sichuan 610106, P.R. China.
Peiling CaiDepartment of Anatomy and Histology, School of Medicine, Chengdu University, Chengdu, Sichuan 610106, P.R. China.
Chengdu University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dihydroartemisinin (DHA) has been shown to inhibit the viability of various cancer cells. Previous studies have revealed that the mechanisms involved in the inhibitory effects of DHA are based on theactivation of p53 and the mitochondrial-related cell death pathway. However, the exact association between upstream signaling and the activation of cell death pathway remains unclear. In this study, we found that DHA treatment induced the upregulation of caveolin 1 (Cav1) and mitochondrial carrier homolog 2 (MTCH2) in HeLa cells, and this was associated with the DHA-induced inhibition of cell viability and DHA-induced apoptosis. Additionally, the overexpression of Cav1 and MTCH2 in HeLa cells enhanced the inhibitory effects of DHA on cell viability. Moreover, we also found that the upregulation of Cav1 contributed to the DHA-mediated p53 activation and the downregulation of the redox enzyme, NAD(P)H:quinone oxidoreductase 1 (NQO1), which have been reported to contribute to the activation of the cell death pathway. Of note, we also found that DHA induced the nuclear translocation and accumulation of both Cav1 and p53, indicating a novel potential mechanism, namely the regulation of p53 activation by Cav1. On the whole, our study identified Cav1 and MTCH2 as the molecular targets of DHA and revealed a new link between the upstream Cav1/MTCH2 upregulation and the downstream activation of the cell death pathway involved in the DHA-mediated inhibition of cell viability.

Indexed as

ArtemisininsCaveolin 1Cell SurvivalFemaleGene Expression Regulation, NeoplasticHeLa CellsHumansMitochondrial Membrane Transport ProteinsNAD(P)H Dehydrogenase (Quinone)Tumor Suppressor Protein p53Up-RegulationUterine Cervical NeoplasmsArtemisininsartenimolCAV1 protein, humanCaveolin 1Mitochondrial Membrane Transport ProteinsMTCH2 protein, humanNAD(P)H Dehydrogenase (Quinone)NQO1 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28498397
PMCPMC5466377
OpenAlexW2612878371

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.