ArticleOncology letters2022
Artemether inhibits proliferation, invasion and migration of hepatocellular carcinoma cells via targeting of CYP2J2.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Artemisinin and Its Derivatives as Potential Anticancer Agents.Molecules (Basel, Switzerland) · 2024Review
- Synthesis of Artemether-Loaded Albumin Nanoparticles and Measurement of Their Anti-Cancer Effects.Biomedicines · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Artemether, a natural derivative of artemisinin, serves an antitumor role in numerous types of cancer. However, the role and mechanism of action of artemether in hepatocellular carcinoma (HCC) has remained elusive. The present study aimed to investigate whether artemether is able to inhibit the proliferation, invasion and migration of HCC cells by targeting cytochrome P450 family 2 subfamily J member 2 (CYP2J2). Cell Counting Kit-8 (CCK-8) and colony-formation assays were used to examine cell viability. Wound-healing and Transwell assays were used to evaluate the cell invasion and migration ability. The expression levels of the epithelial-mesenchymal transition-related proteins E-cadherin, N-cadherin and vimentin were detected via western blot analysis. To determine the mechanism of the inhibitory effect of artemether on HCC, CYP2J2 was overexpressed and its expression in cells treated with artemether was confirmed using reverse transcription-quantitative PCR and western blot analysis. The effects of artemether on the viability, proliferation and migration of HCC cells overexpressing CYP2J2 were detected using CCK-8, colony-formation, wound-healing and Transwell assays, respectively. Artemether was demonstrated to exert a significant inhibitory effect on the proliferation, invasion and migration of HCC cells. Furthermore, artemether also inhibited CYP2J2 expression in Hep3B2.1-7 cells and CYP2J2 overexpression reversed the inhibitory effect of artemether on the proliferation, invasion and migration of HCC cells. Overall, these results indicated that artemether may inhibit HCC cell proliferation, invasion and migration via targeting CYP2J2. These findings may provide potential targets for future HCC therapeutics.
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