Abstract
Farnesyltransferase inhibitors (FTIs) were designed to block the action of Ras oncoproteins which depend on posttranslational modification by adding a farnesyl isoprenoid membrane anchor. However, off-target actions are believed to account for most of their antitumor activity. We recently reported the induction of autophagy in cancer cells in a dose-dependent manner by FTIs. We observed similar results of autophagy in a panel of tumor cell lines for the three FTIs tested. Therefore, the induction of autophagy is very likely a pharmacological class effect of inhibition of farnesyltransferase. In this addendum, we discuss the possible mechanisms underlying the induction of autophagy by FTIs, including reactive oxygen species-, DNA damage- and Ras-mediated pathways as alternatives to Rheb-mediated regulation of mTOR and autophagy.
Original language | English (US) |
---|---|
Pages (from-to) | 129-131 |
Number of pages | 3 |
Journal | Autophagy |
Volume | 5 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2009 |
Keywords
- Autophagy
- DNA damage
- Farnesyltransferase inhibitor
- Ras
- Reactive oxygen species
- Rheb
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology