ArticleOncotarget2017
Oridonin synergistically enhances JQ1-triggered apoptosis in hepatocellular cancer cells through mitochondrial pathway.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Chromatin chronicles: Unlocking the therapeutic potential of histone modifiers in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- Elucidating the Mechanism of Oridonin in Treating Hepatocellular Carcinoma: Network Pharmacology and Experimental Validation.Journal of cellular and molecular medicine · 2026Article
- Targeting the NLRP3 inflammasome for inflammatory disease therapy.Trends in pharmacological sciences · 2025Review
- A Potential Role for Oridonin in Cancer Control: Mechanisms of Autophagy and Apoptosis.Current cancer drug targets · 2025Review
- Oridonin suppresses gastric cancer SGC-7901 cell proliferation by targeting the TNF-alpha/androgen receptor/TGF-beta signalling pathway axis.Journal of cellular and molecular medicine · 2023Article
- Recent advances in oridonin derivatives with anticancer activity.Frontiers in chemistry · 2023Review
- Oridonin and its derivatives for cancer treatment and overcoming therapeutic resistance.Genes & diseases · 2021Review
- Investigation of Metal-Organic Framework-5 (MOF-5) as an Antitumor Drug Oridonin Sustained Release Carrier.Molecules (Basel, Switzerland) · 2019Article
- Function of BRD4 in the pathogenesis of high glucose‑induced cardiac hypertrophy.Molecular medicine reports · 2019Article
- Antifibrosis Effect of Novel Oridonin Analog CYD0618 Via Suppression of the NF-κB Pathway.The Journal of surgical research · 2018Article
- Arsenic sulfide amplifies JQ1 toxicity via mitochondrial pathway in gastric and colon cancer cells.Drug design, development and therapy · 2018Article
- Nanodelivery systems and stabilized solid-drug nanoparticles for orally administered medicine: current landscape.International journal of nanomedicine · 2018Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bromodomain and Extra-Terminal Domain (BET) inhibitors, such as JQ1 have emerged as novel drug candidates and are being enthusiastically pursued in clinical trials for the treatment of cancer. However, many solid cancers are resistance to BET inhibitors. To explore methods for improving the therapeutic potential of BET inhibitors, we investigated the combinational activity of JQ1 with Oridonin, a bioactive molecules derived from Traditional Chinese Medicine in hepatocellular carcinoma (HCC) cells. Our results showed that Oridonin synergistically enhanced the abilities of JQ1 to inhibit cell viability in HCC cells and, significantly augmented JQ1-triggered apoptosis in HCC cells and in HCC cancer stem-like cells. Moreover, Oridonin dose-dependently inhibited the expression of several anti-apoptotic proteins, such as Bcl-2, Mcl-1, and x-linked inhibitor of apoptosis (xIAP) in HCC cells. Cell fractionation and western blotting analysis showed that the enhancement of apoptosis by Oridonin was associated with cytochrome c release, activation of caspase-9, -3 and cleavage of PARP, indicating the activation of mitochondrial apoptosis pathway. Altogether, our findings demonstrate that Oridonin may be used to effectively enhance the sensitivity of BET inhibitors in HCC therapy via downregulation of the expression of multiple anti-apoptotic proteins.
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