Metabolic Reprogramming by c-MET Inhibition as a Targetable Vulnerability in Glioblastoma

Trang Thi Thu Nguyen1, Enyuan Shang2, Georg Karpel-Massler3, Markus D. Siegelin1

1 Department of Pathology & Cell Biology, Columbia University Medical Center, New York, New York, U.S.A.

2 Department of Biological Sciences, Bronx Community College, City University of New York, Bronx, New York, NY., U.S.A.

3 Department of Neurosurgery, Ulm University Medical Center, Ulm, Germany.

Correspondence to:

Markus D. Siegelin, email:ms4169@cumc.columbia.edu

Keywords:c-MET; Metabolic Reprogramming; Fatty Acid Oxidation; Glioblastoma

Received: March 04, 2020 Accepted: March 05, 2020 Published: March 20, 2020


The elucidation of better treatments for solid tumors and especially malignant glial tumors is a priority. Better understanding of the molecular underpinnings of treatment response and resistance are critical determinants in the success for this endeavor. Recently, a battery of novel tools have surfaced that allow to interrogate tumor cell metabolism to more precise extent than this was possible in the earlier days. At the forefront of these developments are the extracellular flux and carbon tracing analyses. Through utilization of these techniques our group made the recent observation that acute and chronic c-MET inhibition drives fatty acid oxidation that in turn can be therapeutically targeted for drug combination therapies. Herein, we summarize and comment on some of our key findings related to this study.

PII: 498