ArticleNaunyn-Schmiedeberg's archives of pharmacology2023
mRNA sequencing and CyTOF analysis revealed ASPP2 altered the response patterns of hepatocellular carcinoma HepG2 cells to usnic acid.
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 1 paper.
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
1 citing paper in PubMed, 2 citations in OpenAlex.
- Retinoic acid generates a beneficial microenvironment for liver progenitor cell activation in acute liver failure.Hepatology communications · 2024Article
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 at 2 institutions in 1 country.
Funding
Abstract
In a previous study, our team found that ASPP2 overexpression increases the sensitivity of liver cancer cells to sorafenib. ASPP2 is an important target in the study of drug therapy for hepatocellular carcinoma. In this study, we demonstrated that ASPP2 altered the response of HepG2 cells to usnic acid (UA) by using mRNA sequencing and CyTOF. CCK8 assay was used to detect cytotoxicity of UA on HepG2 cells. Annexin V-RPE assay, TUNEL assay, and cleaved caspase 3 assay were performed to examine the apoptotic cell death induced by UA. Transcriptomic sequencing and a single-cell mass cytometry were used to analyze the dynamic response of HepG2shcon and HepG2shASPP2 cells to UA treatment. We have demonstrated that UA could inhibit proliferation in HepG2 cells in a concentration-dependent manner. Apoptotic cell death was significantly induced by UA in HepG2 cells, while knocking down ASPP2 could increase the resistance of HepG2 cells to UA. Data from mRNA-Seq indicated that knockout of ASPP2 in HepG2 cells affected cell proliferation, cycle, and metabolism. ASPP2 knockdown resulted in increased stemness and decreased apoptosis of HepG2 cells under the action of UA. CyTOF analysis confirmed the above results, ASPP2 knockdown increased oncoproteins in HepG2 cells and altered response patterns of HepG2 cells to UA. Our data suggested that the natural compound UA could inhibit liver cancer HepG2 cells; meanwhile, ASPP2 knockdown could affect response patterns of HepG2 cells to UA. The above results indicate that ASPP2 could be a research target in the chemoresistance of liver cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.