Evidence map›Paper›PMID 32831913›Full record

ArticleOncology letters2020

Dihydroartemisinin inhibits the migration of esophageal cancer cells by inducing autophagy.

Xiao Chen, Lan-Ying He, Shu Lai, Yao He

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 25 citations in OpenAlex.

  1. The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Autophagy and its role in gastrointestinal diseases.World journal of gastroenterology · 2024
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Autophagy in gastrointestinal cancers.Frontiers in oncology · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Dihydroartemisinin: A Potential Natural Anticancer Drug.International journal of biological sciences · 2021
    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 4 institutions in 1 country.

Xiao ChenDepartment of Pharmacy, Chongqing Emergency Medical Center, Chongqing University Central Hospital, Chongqing 400014, P.R. China.
Lan-Ying HeDepartment of Gastroenterology, Tumor Hospital Affiliated to Chongqing University, Chongqing 400030, P.R. China.
Shu LaiDepartment of Pharmacy, Jiulongpo District People's Hospital of Chongqing, Chongqing 400050, P.R. China.
Yao HeDepartment of Pharmacy, Chongqing Emergency Medical Center, Chongqing University Central Hospital, Chongqing 400014, P.R. China.
Chongqing Cancer Hospital · CNChongqing Emergency Medical Center · CNChongqing Jiulongpo People's Hospital · CNChongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer (EC) is a complex gastrointestinal malignancy and its global incidence rate ranks 7th among all cancer types. Due to its aggressive nature and the potential for early metastasis, the survival rates of patients with EC are poor. Dihydroartemisinin (DHA) is the primary active derivative of artemisinin, and, as well as its use as an anti-malarial, DHA has also exhibited antitumor activity in various cancer models, such as cholangiocarcinoma, head and neck carcinoma, and hepatocellular carcinoma cells. However, the molecular mechanisms underlying the antitumor effect of DHA in the treatment of EC remains poorly understood. The results of the present study demonstrated that DHA significantly inhibited the migration of TE-1 and Eca-109 EC cells in a dose-dependent manner by activating autophagy. DHA treatment also significantly reversed epithelial-mesenchymal transition (EMT) by downregulating the EMT-associated markers, N-cadherin and vimentin, and upregulating the expression of E-cadherin. Mechanistically, DHA treatment decreased Akt phosphorylation and inhibited the Akt/mTOR signaling pathway, leading to the activation of autophagy. The levels of the autophagy-associated proteins were suppressed and DHA-mediated inhibition of migration in EC cells was reversed when an active form of Akt was overexpressed. In conclusion, the present study demonstrated the potential value of DHA in the treatment of EC, and revealed the underlying mechanism by which FDHA inhibits cellular migration.

Indexed as

Aktautophagydihydroartemisininesophageal cancermigration

Identifiers

PMID32831913
PMCPMC7439151
OpenAlexW3047923341

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.