Ras inhibition enhances autophagy, which partially protects cells from death
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Eran Schmukler1, Efrat Grinboim1, Sari Schokoroy1, Adva Amir1, Eya Wolfson1, Yoel Kloog1 and Ronit Pinkas-Kramarski1
1 Department of Neurobiology, Tel-Aviv University, Ramat-Aviv, Israel
Ronit Pinkas-Kramarski, email:
Keywords: autophagy, Ras, transformation, signal transduction.
Received: October 09, 2012, Accepted: January 17, 2013, Published: January 19, 2013
Autophagy, a process of regulated turnover of cellular constituents, is essential for normal growth control but may be defective under pathological conditions. The Ras/PI3K/mTOR signaling pathway negatively regulates autophagy. Ras signaling has been documented in a large number of human cancers. In this in-vitro study we examined the effect of the Ras inhibitor Salirasib (S-trans, trans-farnesylthiosalicylic acid; FTS) on autophagy induction and cell viability. We show that Ras inhibition by FTS induced autophagy in several cell lines, including mouse embryonic fibroblasts and the human cancer cell lines HeLa, HCT-116 and DLD-1. The autophagy induced by FTS seems to inhibit the cell death induced by FTS, since in the absence of autophagy the death of FTS-treated cells was enhanced. Therefore, inhibition of autophagy may promote the inhibition of tumor cell growth and the cell death mediated by FTS.
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