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Targeting the protein prenyltransferases efficiently reduces tumor development in mice with K-RAS-induced lung cancer

Meng Liu1, Anna-Karin M Sjogren, Christin Karlsson

  • 1Wallenberg Laboratory, Institute of Medicine, Sahlgrenska University Hospital, S-41345 Gothenburg, Sweden.

Proceedings of the National Academy of Sciences of the United States of America
|March 24, 2010
PubMed

Insights

Inactivating protein farnesyltransferase (FTase) and protein geranylgeranyltransferase-I (GGTase-I) genetically reduced lung tumors. Simultaneous genetic inhibition of FTase and GGTase-I shows promise for cancer therapeutics.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • RAS and RHO proteins are crucial in tumorigenesis and metastasis.
  • Posttranslational modification by FTase or GGTase-I affects these proteins.
  • Previous attempts to inhibit FTase/GGTase-I faced challenges like off-target effects and toxicity.

Purpose of the Study:

  • To evaluate the impact of FTase deficiency and combined FTase/GGTase-I deficiency using genetic approaches.
  • To explore the therapeutic potential of simultaneous FTase and GGTase-I inhibition in cancer.

Main Methods:

  • Genetic inactivation of FTase in cell cultures and mouse models.
  • Assessment of protein farnesylation, protein localization, and cell proliferation.
  • Evaluation of tumor growth and survival in K-RAS-induced lung cancer models.
  • Combined genetic inactivation of FTase and GGTase-I.

Main Results:

  • FTase inactivation prevented H-RAS farnesylation and plasma membrane targeting, inhibiting fibroblast proliferation.
  • FTase inactivation in mice reduced lung tumor growth and improved survival.
  • Simultaneous inactivation of FTase and GGTase-I significantly reduced lung tumors and improved survival with no apparent pulmonary toxicity.

Conclusions:

  • FTase plays a significant biochemical and therapeutic role in cancer.
  • Simultaneous genetic inhibition of FTase and GGTase-I is a promising strategy for cancer therapeutics.
  • This approach may overcome limitations of previous inhibitor-based strategies.

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