ArticleNaunyn-Schmiedeberg's archives of pharmacology2023
Integrating network pharmacology and experimental models to examine the mechanisms of corosolic acid in preventing hepatocellular carcinoma progression through activation PERK-eIF2a-ATF4 signaling.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2023. 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.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- A review of the pharmacological mechanism of corosolic acid.Frontiers in pharmacology · 2026Review
- Hawthorn with "homology of medicine and food": a review of anticancer effects and mechanisms.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the most prevalent form of liver cancer, with a high recurrence rate and heterogeneity. We aimed to examine the effect of corosolic acid (CRA) on HCC. We employed transcriptomics to validate the target molecules in CRA-treated HCC cells and conducted enrichment analyses that revealed their involvement in the regulation of endoplasmic reticulum (ER) stress and apoptosis. Our experimental data indicated that CRA markedly induced apoptosis in human HCC cell lines through the mitochondrial apoptosis pathway. We also revealed that the pro-apoptotic effects of CRA depended on ER stress, as pretreatment with selective ERS inhibitor salubrinal effectively reversed CRA-induced cell apoptosis. Furthermore, the knockdown of the unfolded protein response (UPR) protein CHOP remarkably abrogated CRA-induced expression of ER stress-associated proteins. Collectively, our results suggest that CRA triggers ER stress-mediated apoptosis in HCC cells via activation of the PERK-eIF2a-ATF4 pathway. Our findings provide novel insights into the potential therapeutic strategies for HCC.
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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.