Lausanne: RasGAP derived peptide for selective killing of cancer cells

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Scientists at Lausanne University have developed a new technology for improving cancer treatments by increasing the efficacy of currently used anti-tumor genotoxins.

They have shown that that the caspase substrate RasGAP can induce both anti- and pro-apoptotic signals, depending on the extent of its cleavage by caspases. A peptide derived from the N-terminal fragment of RasGAP fused to the TAT cell permeation sequence (TAT∙RasGAP317-326) has been shown to enhance apoptosis of tumors cells induced by various genotoxins such as cisplatin, adryamycin and mitoxantrone.

The recombinant peptide TAT∙RasGAP317-326 could inhibit the in vitro proliferation of 5 cancer cell lines: Hela cells (human adenocarcinoma), MCF-7 cells (breast cancer), U2OS (human osteosarcoma), H-Meso-1 (human malignant mesothelomia) and HCT116 (human colon carcinoma).

The recombinant peptide TAT∙RasGAP317-326 in combination with cisplatin has also been shown to inhibit the proliferation of established tumors in mice more efficiently than cisplatin alone at doses devoid of side effects and 100 times lower than lethal doses.

The results obtained with the RasGAP317-326 peptide offer the possibility to improve cancer treatments by:

• enhancing the effect of genotoxins specifically in tumor cells

• allowing efficient tumor treatment and reduced side-effects by using lower doses of genotoxins

• preventing the outgrowth of genotoxin-resistant tumors