ArticleCell death & disease2018
Caspase-3 suppresses diethylnitrosamine-induced hepatocyte death, compensatory proliferation and hepatocarcinogenesis through inhibiting p38 activation.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
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- Network-Pharmacology-Based Study on Active Phytochemicals and Molecular Mechanism ofInternational journal of molecular sciences · 2022Article
- Ameliorative potential of manganese nanoparticles with low-level ionizing radiation against experimentally induced hepatocarcinogenesis.Environmental science and pollution research international · 2021Article
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- Loss of PGRMC1 Delays the Progression of Hepatocellular Carcinoma via Suppression of Pro-Inflammatory Immune Responses.Cancers · 2021Article
- Adamantane-linked isothiourea derivatives suppress the growth of experimental hepatocellular carcinomaAmerican journal of cancer research · 2021Article
- PITPNC1 fuels radioresistance of rectal cancer by inhibiting reactive oxygen species production.Annals of translational medicine · 2020Article
- miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling.Frontiers in neurology · 2020Article
- Systematic Elucidation of the Potential Mechanisms of Core Chinese Materia Medicas in Treating Liver Cancer Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- MicroRNA-562 negatively regulated c-MET/AKT pathway in the growth of glioblastoma cells.OncoTargets and therapy · 2019Article
- Restriction of H1N1 influenza virus infection by selenium nanoparticles loaded with ribavirin via resisting caspase-3 apoptotic pathway.International journal of nanomedicine · 2018Article
- Potential targets of TMEM176A in the growth of glioblastoma cells.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
It is critical to understand the molecular mechanisms of hepatocarcinogenesis in order to prevent or treat hepatocellular carcinoma (HCC). The development of HCC is commonly associated with hepatocyte death and compensatory proliferation. However, the role of Caspase-3, a key apoptotic executor, in hepatocarcinogenesis is unknown. In this study, we used Caspase-3-deficient mice to examine the role of Caspase-3 in hepatocarcinogenesis in a chemical (diethylnitrosamine, DEN)-induced HCC model. We found that Caspase-3 deficiency significantly increased DEN-induced HCC. Unexpectedly, Caspase-3 deficiency increased apoptosis induced by DEN and the subsequent compensatory proliferation. Intriguingly, we discovered that Caspase-3 deficiency increased the activation of p38 with and without DEN treatment. Moreover, we demonstrated that TNFα and IL1α stimulated increased activation of p38 in Caspase-3 KO hepatocytes compared with wild-type hepatocytes. Finally, we found that inhibition of p38 by SB202190 abrogated enhanced hepatocyte death, compensatory proliferation and HCC induced by DEN in Caspase-3-deficient mice. Overall, our data suggest that Caspase-3 inhibits chemical-induced hepatocarcinogenesis by suppressing p38 activation and hepatocyte death.
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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.