ArticleCytotechnology2025
Dihydroartemisinin suppresses COX-2-mediated apoptosis resistance in hepatocellular carcinoma under endoplasmic reticulum stress.
Article in Cytotechnology, 2025. 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
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.
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.
- The Therapeutic Potential of Dihydroartemisinin in Cancer Treatment.International journal of molecular sciences · 2026Review
- The interaction between COX-2 and endoplasmic reticulum stress is involved in liver ischemia-reperfusion injury in mice.Molecular biology reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, and its treatment still faces numerous challenges. Dihydroartemisinin (DHA), a derivative of artemisinin, has shown significant antitumor activity in preclinical research. Our study seeks to uncover the molecular mechanisms of DHA in HCC, potentially providing scientific evidence for its use as a supportive therapy in clinical settings. This study was conducted using various experimental approaches to systematically analyze the effects of DHA in HCC. Cell viability was evaluated by CCK-8 to determine the IC
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Registered trials
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.