Fig. 4. CME induces anti-proliferation effects, apoptosis and cell cycle arrest at G1 phase via regulating Akt/GSK-3β/mTOR and Akt/GSK-3β/β-catenin signaling pathways. Cells were treated with 20 μM LY294002 or 1 μM BIO or 20 μM Celecoxib or 1 μM XAV939 or 60 μg/mL CME for 24 h. (a) Cell viability was measured by MTT assay. The statistical analysis of the data was carried out by use of independent sample t-test. *p < 0.05, **p < 0.01 and ***p < 0.001 vs. con. ##p < 0.01 and ###p < 0.001 vs. CME-treated group (each experiment, n = 3). (b) LDH release was measured by LDH release assay. The statistical analysis of the data was carried out by use of independent sample t-test. **p < 0.01 and ***p < 0.001 vs. con. #p < 0.05 and ###p < 0.001 vs. CME-treated group (each experiment, n=3). (c) Apoptotic effects of CME were evaluated by Annexin V-PI staining. (d) Cell cycle arrest effects were measured by flow cytometric. N.S., not significant; CME, Cnidium monnieri (L.) Cusson extract; con, control.
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