Turning off the tap for tumors: STAT3 protein fuels neoplastic growth

Mitochondrial Stat3 Supports Ras-Dependent Oncogenic Transformation
Science, June 26, 2009: Vol. 324. no. 5935, pp. 1713-1716

Daniel J. Gough¹*, Alicia Corlett^1,3*, Karni Schlessinger^1,4, Joanna Wegrzyn², Andrew C. Larner², and David E. Levy^1
1Department of Pathology and NYU Cancer Institute, New York University School of
Medicine, 550 First Avenue, New York, NY 10016, USA.
²Department of Biochemistry and Massey Cancer Center, Virginia Commonwealth
University, Richmond, VA 23298, USA.
³Institute of Molecular Genetics AS CR, v.v.i., Vídeňská 1083, Prague 4, Czech Republic 14220.
⁴Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA.
*These authors contributed equally to this work.
Correspondence: David.Levy@med.nyu.edu


The Levy lab reports that a protein, known as STAT3, is required for the growth of at least some tumors. It was previously thought that this protein functioned only in the cell nucleus, where it acts as a transcription factor to regulate gene expression. But now the Levy Lab has found that it is also present in mitochondria, the energy-generating organelle of the cell. It has long been known that tumor metabolism is highly dependent on the simple sugar glucose for energy, and the Levy lab has now shown that STAT3 contributes to tumor-specific metabolic processes. When STAT3 was removed from tumor cells, they underwent a metabolic shift that impaired their ability to grow as solid tumors. In contrast, normal cells were not adversely affected in this manner by loss of STAT3. This observation may open an avenue to a novel therapeutic approach to cancer, by inhibiting the mitochondrial-specific function of STAT3 to deprive tumors of a necessary energy source.

Read the related press release by the NYU Langone Medical Center Office of Communications and Public Affairs.