ArticleJapanese journal of cancer research : Gann2002
Beta-hydroxyisovalerylshikonin is a novel and potent inhibitor of protein tyrosine kinases.
Article in Japanese journal of cancer research : Gann, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 36 citations in OpenAlex.
- Volatile Natural Deep Eutectic Solvents (VNADESs) for Extraction of Shikonin Derivatives fromMolecules (Basel, Switzerland) · 2026Article
- Shikonin Exerts an Antileukemia Effect against FLT3-ITD Mutated Acute Myeloid Leukemia Cells via Targeting FLT3 and Its Downstream Pathways.Acta haematologica · 2024Article
- Beta-Hydroxyisovaleryl-Shikonin Eradicates Epithelial Cell Adhesion Molecule-Positive Liver Cancer Stem Cells by Suppressing dUTP Pyrophosphatase Expression.International journal of molecular sciences · 2023Article
- Shikonin and Juglone InhibitBiotech (Basel (Switzerland)) · 2023Article
- β-hydroxyisovaleryl-shikonin induces human cervical cancer cell apoptosis via PI3K/AKT/mTOR signaling.Oncology letters · 2015Article
- Targeting epidermal growth factor receptors and downstream signaling pathways in cancer by phytochemicals.Targeted oncology · 2015Review
- Mechanism of inhibition of tumor angiogenesis by beta-hydroxyisovalerylshikonin.Cancer science · 2009Article
- Cyclooxygenase-2 inhibitory effects and composition of the volatile oil from the dried roots of Lithospermum erythrorhizon.Journal of natural medicines · 2008Article
- Beta-hydroxyisovalerylshikonin induces apoptosis in human leukemia cells by inhibiting the activity of a polo-like kinase 1 (PLK1).Oncogene · 2003Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta-hydroxyisovalerylshikonin (beta-HIVS), a compound isolated from Lithospermium radix, most efficiently induced cell-death in two lines of lung cancer cells, namely, NCI-H522 and DMS114, whereas shikonin was effective against a wide variety of tumor cell lines. During our studies of the mechanism of action of beta-HIVS on tumor cells, we found that this compound inhibited protein tyrosine kinase (PTK) activity. The tyrosine kinase activities of a receptor for EGF (EGFR) and v-Src were strongly inhibited and that of KDR/Flk-1 was weakly inhibited by beta-HIVS. The inhibition by beta-HIVS of the activities of EGFR and v-Src was much stronger than that by shikonin. The IC50 values of beta-HIVS for EGFR and v-Src were approximately 0.7 microM and 1 microM, respectively. Moreover, the inhibition of v-Src by beta-HIVS was non-competitive with respect to ATP. These results strongly suggest that the action of beta-HIVS, as well as that of shikonin, involves the inhibition of PTK, and they also suggest the possibility of producing a novel group of PTK inhibitors based on shikonin as the parent compound.
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