Using a mouse tumor model, the tumor-progression capacity of transfected and untransfected SW1990 cells was investigated, indicating that DLC-1 transfection reduced the capacity for tumor progression.
Together, our findings indicate that complex formation between the DLC1 START domain and CAV-1 contributes to DLC1 tumor suppression via a RhoGAP-independent mechanism, and suggest that DLC1 inactivation probably contributes to cancer progression.
These observations implicate the DLC1 gene in suppression of HCC cell dissemination and identify novel cellular and genetic alterations that contribute to prevention of metastasis, a life-threatening event in cancer progression.