casticin and Carcinoma--Squamous-Cell

Casticin expresses multiple anti-cancer activities, whereas the effect of casticin on oral squamous cell carcinoma (OSCC) is still unclear. β-catenin signaling plays a crucial role in the epithelial-mesenchymal transition which is closely related to tumorigenesis. Herein, we aimed to study the functions of casticin on invasion and migration of OSCC, and clarify whether the effect of casticin on OSCC has a relationship with β-catenin signaling.. Human OSCC cell lines UM1 and HSC-3 were treated with different concentrations of casticin. The cell viability was evaluated by MTT and soft agar colony formation. Transwell assay and wound-healing assay were performed to measure the ability of cell invasion and migration. The protein expression was assessed by Western blotting.. Casticin displayed inhibitory activities of cell viability, invasion, and migration on OSCC cell lines. Meanwhile, casticin could reverse EMT process and inhibit the expression of β-catenin in OSCC. Knock-down or overexpression of β-catenin could alter the effect of casticin on OSCC.. Casticin impaired invasion and migration of OSCC by inhibition of β-catenin and reversal of EMT and could be a potential anti-cancer bioactive agent.

Topics: beta Catenin; Carcinoma, Squamous Cell; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Down-Regulation; Epithelial-Mesenchymal Transition; Flavonoids; Humans; Mouth Neoplasms; Neoplasm Invasiveness; Signal Transduction

Flavonoids are distributed in many plants. We studied the antitumor effects of flavonoids isolated from Viticis Fructus, casticin, artemetin, quercetagetin and 5,3'-dihydroxy-6,7,4' -trimethoxyflavanone. Casticin inhibited the growth of KB cells markedly (IC(50)=0.23 microM), compared with the other flavonoids tested (IC(50)=15.3-18.6 microM). In contrast, casticin did not inhibit the proliferation of A431 cells similar to normal cell lines, 3T3 Swiss Albino and TIG-103. Flow cytometric analyses revealed that the exposure of KB cells to casticin led to significant arrest at G2-M. In immunostaining of KB cells, casticin disrupted mitotic spindles. These results suggest that G2-M arrest by casticin may be relevant to its antimitotic activity, although the mechanism of selective growth inhibition has been unknown. Further examinations are required to confirm that casticin is an antitumor drug for specific cancers with low toxicity.

Topics: Aldehyde Reductase; Animals; Carcinoma, Squamous Cell; Cell Division; Cells, Cultured; Chromones; Flavones; Flavonoids; G2 Phase; Humans; KB Cells; Mice; Mitosis; Spindle Apparatus; Swiss 3T3 Cells; Vitex