IMR Press / FBL / Volume 13 / Issue 2 / DOI: 10.2741/2701

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article

Shikonin analogue (SA) 93/637 induces apoptosis by activation of caspase-3 in U937 cells

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1 Center for Combat Casualty and Life Sustainment Research, Department of Pathology, Uniformed Services University of the Health Sciences (USUHS), Bethesda, MD 20814, USA
2 Birla Institute of Technology and Science, Pilani 333031, India
3 Central Drug Research Institute, Lucknow 226001, India
Front. Biosci. (Landmark Ed) 2008, 13(2), 561–568; https://doi.org/10.2741/2701
Published: 1 January 2008
Abstract

β,β-dimethyl acryl shikonin is an extract from the root of plant Arnebia nobilis which has been shown to possess anti-cancer activity. However, its toxicity limited further development of shikonin as a therapeutic agent. Subsequently, several analogues of β,β-dimethyl acryl shikonin were synthesized. One of these analogues, shikonin 93/637 was found to be significantly less toxic compared to shikonin. This study is aimed to determine the cell cycle associated differences in the susceptibility of U937 cells to apoptosis induced by shikonin analogue 93/637 (SA). Lower concentrations of SA (~100nM) showed no significant changes in cell growth. However, higher concentrations (~500nM) resulted in growth inhibition of U937 cells after 48 h of treatment with SA as measured by MTT assay. Flow cytometric analysis showed that SA treatment resulted in blocking of cell cycle progression in G1 phase. Decreased expression of Cyclin D, CDK 4 and PCNA was observed with SA treatment corroborating the G1 block. DNA gel electrophoresis showed an oligonucleotide ladder pattern, a distinct characteristic of DNA fragmentation associated with programmed cell death. Ribonuclease protection assay revealed inhibition of bcl2 expression at transcriptional level. SA treatment also resulted in induction of caspase-3 activity. The results suggest the involvement of bcl2 and Caspase-3 in SA induced apoptosis of human U937 cells.

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