Molecular-targeting chemotherapy related to p53-RB for malignant bone and soft tissue tumors

MEK抑制剂抑制纤维肉瘤细胞的生长，并以剂量依赖性方式增加G1/S期细胞的数量。ERK磷酸化受到抑制，p21^WAF1/CIP 1和p27^KIP1蛋白表达增加。萝卜硫素（Sulforaphane，SFN）通过抑制ERK和Akt的活化，诱导骨肉瘤细胞G2/M期阻滞，诱导细胞凋亡，从而增强骨肉瘤细胞的放射敏感性。这些结果表明，SFN可作为骨肉瘤的放射增敏剂。

A MEK inhibitor suppressed cell growth and increased the population of G1/S phase cells in a dose-dependent manner for fibrosarcoma cells. The phosphorylation of ERK was inhibited and p21^WAF1/CIP1 and p27^KIP1 protein expression increased. These results indicate that it might be an attractive compound for molecular-targeting chemotherapy with the activation of the Ras-MEK-ERK pathway.Sulforaphane(SFN) enhanced the radiosensitivity of osteosarcoma cells by inducing apoptosis through G2/M-phase arrest and inhibiting ERK and Akt activation. These findings suggest that SFN can be used as a radiosensitizer for osteosarcomas.