Ras inhibition enhances autophagy, which partially protects cells from death

Eran Schmukler, Efrat Grinboim, Sari Schokoroy, Adva Amir, Eya Wolfson, Yoel Kloog, Ronit Pinkas-Kramarski

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)145-155
Number of pages11
Issue number1
StatePublished - 2013


  • Autophagy
  • Ras
  • Signal transduction
  • Transformation

All Science Journal Classification (ASJC) codes

  • Oncology


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