Abstract
Background: Recent studies have shown that increased dietary consumption of flavones and isoflavones is associated with reduced risk of developing cancer. Natural plants/herbs used in Traditional East Asian
Medicine (TEAM) have been recognized as potentially efficacious natural treatments against cancer and are enriched with isoflavones and flavones, as well as other interesting compounds. We used a novel high throughput screening method to identify natural extracts that may have a potential anti-cancer effect and identified the TEAM natural product Scutellaria baicalensis and a known active component, the flavone, baicalein. The objective of our current study is to investigate the anti-cancer effects of baicalein in vitro and in vivo.
Methods: In vitro testing was performed in mouse (C3L5) and human (SKBR3) breast cancer cell lines. Cell viability was assessed by MTT assay. Apoptosis was assessed using FITC-Annexin V and PI staining with bivariate reading by flow cytometry at 48 h. A syngeneic mouse breast cancer model (C3H/HeJ — C3L5) was used for in vivo testing. Mice bearing subcutaneous tumors were either treated with daily intraperitoneal injection of vehicle or baicalein (20 mg/kg) five days a week for three weeks (n=6/group). Tumor size and weights were measured.
Results: Baicalein had a marked cytotoxic effect in C3L5 cells with an IC50 of less than 10mM (data not shown). FITC-Annexin V and PI analysis with flow cytometry for C3L5 cells treated at 10μM for 48h showed a marked increase in the Annexin V positive fraction indicative of apoptosis.
In vivo studies demonstrated a significantly decreased tumor growth in mice treated with intraperitoneal baicalein when compared to the control group (P<0.05).
Baicalein treated cells demonstrated STAT3 inhibition on western blot analysis by decreased presence of phospho-STAT3 (data not shown).
Conclusions: Baicalein, a flavone from TEAM demonstrates significant anti-cancer effects due to apoptosis in breast cancer. STAT3, a well-known anti-apoptotic signaling intermediate, is inhibited in activation as reflected by decreased phosphoSTAT3 which may account for these effects.
Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P6-14-13.
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