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Abstract
Additionally, the Hedgehog (Hh) signaling pathway regulates tumor invasion and metastasis, with its mediators Shh and Gli-1 over-expressed in OSCC [7]. [...]the inhibition of collagen fiber degradation in the ECM and BM by MMPs and the modulation of upstream signaling molecules in the Hh pathway may be keys to controlling clinical tumor invasion and migration in OSCC. [...]the limitations of DOX have become increasingly evident: DOX has been shown to be associated with increased incidence of cardiomyopathy, and drug tolerance limits its usage in cancer treatment [14, 15]. [...]the drug is almost undetectable in tumors and their surrounding areas after intravenous administration of DOX to mice, which indicates that DOX has a very low permeability and diffusion potential [16]. [...]an important research goal would be to find a non-invasive approach to improve local drug permeability in OSCC cells. [...]MTT assays showed no effect for normal HT293 cells treated under the same conditions. [...]these results indicate that the increased in vitro cytotoxicity of DOX to human OSCC after ultrasound exposure is associated with increased intracellular DOX.