2HF also depleted the Ral-regulated, stress-responsive,antiapoptotic endocytic protein RLIP76 (RALBP1), the inhibition of which has previously beenshown to inhibit B16-F0 melanoma growth in vivo.
Our previous study involving RLIP76-/- mice implanted with melanoma or carcinoma cell conclusively demonstrated that RLIP76 is necessary for angiogenesis and neovascularization of primary solid tumors.
Moreover, by testing the cell migratory and invasive abilities by wound scratch and transwell assays, it determined that the RLIP76 also suppressed cell migration and invasion in A375 cells and P13K/Akt signalling CONCLUSIONS: Overall, this study suggests that RLIP76 is a potential therapeutic target against melanoma.
Collectively, our findings define RIP1 as an oncogenic driver in melanoma, with potential implications for targeting its NF-κB-dependent activation mechanism as a novel approach to treat this disease.
These findings strongly suggest that RLIP76 depletion by genetic approaches or inhibition by antibodies may be a clinically viable antineoplastic therapy, particularly for melanoma.