Early stages of
melanoma can be successfully treated by surgical resection of the
tumor, but there is still no effective treatment once it is progressed to metastatic phases. Although growing family of both
melanoma metastasis promoting and metastasis suppressor genes have been reported be related to
metastasis, the molecular mechanisms governing
melanoma metastatic cascade are still not completely understood. Therefore, defining the molecules that govern
melanoma metastasis may aid the development of more effective therapeutic strategies for combating
melanoma. In the present study, we found that muc1 is involved in the
metastasis of
melanoma cells and demonstrated that muc1 disruption impairs
melanoma cells migration and
metastasis. The requirement of muc1 in the migration of
melanoma cells was further confirmed by gene silencing in vitro. In corresponding to this result, over-expression of muc1 significantly promoted the migratory of
melanoma cells. Moreover, down-regulation of muc1 expression strikingly inhibits
melanoma cellular
metastasis in vivo. Finally, we found that muc1 promotes
melanoma migration through the
protein kinase B (Akt) signaling pathway. To conclude, our findings suggest a novel mechanism underlying the
metastasis of
melanoma cells which might serve as a new intervention target for the treatment of
melanoma.