Autophagy induced by farnesyltransferase inhibitors in cancer cells

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Jingxuan Pan1, Bo Chen, Chun-Hui Su

  • 1Department of Pathophysiology, Sun Yat-Sen University Medical School, Guangzhou, Guangdong, PR China. jingx_pan@yahoo.com.cn

Cancer Biology & Therapy
|September 5, 2008
PubMed

Insights

Farnesyltransferase inhibitors (FTIs) induce autophagy in cancer cells. Cancer cells may switch between apoptosis and autophagy when treated with FTIs, impacting cell death or survival.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Farnesyltransferase inhibitors (FTIs) act via Rheb and the PI3K/Akt/mTOR pathway.
  • Mammalian target of rapamycin (mTOR) is crucial for regulating autophagy.
  • Previous literature suggests FTIs induce autophagy, but effects on cancer cell biology are unreported.

Purpose of the Study:

  • To investigate if FTIs induce autophagy in human cancer cell lines.
  • To explore the role of autophagy and apoptosis in cancer cell response to FTIs.

Main Methods:

  • Treatment of two human cancer cell lines with FTIs: manumycin A, FTI-276, and lonafarnib.
  • Assessment of autophagy induction by FTIs.
  • Inhibition of apoptosis and autophagy to evaluate their impact on lonafarnib-treated U2OS cell clone formation in soft agar.

Main Results:

  • Manumycin A, FTI-276, and lonafarnib induced autophagy in the tested cancer cell lines.
  • Inhibiting apoptosis or autophagy did not alter the number of lonafarnib-treated U2OS cell clones in soft agar.
  • Cancer cells demonstrated a potential to switch between apoptosis and autophagy following FTI treatment.

Conclusions:

  • FTIs induce autophagy in cancer cells.
  • The precise role of autophagy (cell death vs. survival) in FTI-treated cancer cells remains to be fully elucidated.
  • Cancer cells exhibit plasticity in cell fate pathways (apoptosis and autophagy) upon FTI exposure.

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