ArticleInternational journal of molecular sciences2022
Deoxyshikonin Mediates Heme Oxygenase-1 Induction and Apoptotic Response via p38 Signaling in Tongue Cancer Cell Lines.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Deoxyshikonin inhibits growth and induces apoptosis of hypertrophic scar-derived fibroblasts by downregulating FBXO expression through autophagy.Scientific reports · 2026Article
- Deoxyshikonin inhibits the proliferation, invasion, and tumor immune microenvironment in breast cancer cells by inactivating the PI3K/AKT/NF-κB pathway.Nutrition research and practice · 2026Article
- THC and CBD Induce Heme Oxygenase-1-Dependent Cell Death and Trigger Mitochondrial Dysfunction in Human Melanoma and Cutaneous Squamous Cell Carcinoma Cells.Antioxidants (Basel, Switzerland) · 2026Article
- A Thia-Analogous IndirubinCells · 2023Article
- Apoptotic effect and cell arrest of deoxyshikonin in human osteosarcoma cells through the p38 pathway.Journal of cellular and molecular medicine · 2023Article
- Hemoxygenase-1 Promotes Head and Neck Cancer Cell Viability.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deoxyshikonin (DSK), a phytochemical constituent, has been documented to elicit various oncostatic properties alone or in combination with established therapeutics. However, its role in restraining oral squamous cell carcinoma (OSCC) is mostly unclear. Here, we examined the tumor-suppressive effect of DSK and explored the molecular mechanisms underlying DSK's activities on controlling oral cancer. Our results showed that DSK dose-dependently lessened the cell viability of tongue cancer cell lines, involving induction of cell cycle arrest at the sub-G1 phase and apoptotic cell death. Moreover, a unique signature of apoptosis-related proteins, including augmented nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) expression and caspase activation, was observed in DSK-treated tongue cancer cell lines. Furthermore, DSK-mediated upregulation of HO-1 and cleavage of caspase-9 and -3 were significantly inhibited by pharmacological blockage of p38 kinase. Collectively, these data revealed that DSK halted cell cycle progression and elicited cell apoptosis in tongue cancer cell lines, reshaping a p38-dependent profile of apoptotic proteome. Our findings provided novel insights into the therapeutic implications of a natural compound on the management of OSCC.
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Registered trials
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