Noriko Mori1, Balaji Krishnamachary1, Yelena Mironchik1, and Zaver M. Bhujwalla1,2,3
1The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University, Baltimore, MD, United States, 2The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, Baltimore, MD, United States, 3Department of Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States
1The Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University, Baltimore, MD, United States, 2The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University, Baltimore, MD, United States, 3Department of Radiation Oncology and Molecular Radiation Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, United States
Glutamine (Gln) addiction in pancreatic ductal adenocarcinoma (PDAC) is mediated by oncogenic Kras. Here, for the first time, we identified alterations in choline metabolism with Gln depletion, and confirmed the importance of Gln in PDAC cell survival.
Figure 2: a. Choline metabolite region of representative 1H MR spectra obtained from the aqueous phase of Panc 1 and Pa04C cells. GPC; glycerophosphocholine, PC; phosphocholine, Cho: choline Cells were collected after culturing in Gln +/- medium for 72h. b. Choline metabolite levels in arbitrary unit (A.U.) obtained from 1H MR spectra of the aqueous phase of Panc 1 and Pa04C cells. Values represent mean ± SEM, ** P ≤ 0.01, * P ≤ 0.05 (n=3).
Figure 1: Panc 1, Pa04C, Pa09C and Pa20C cell numbers with or without Gln depletion. ~105 cells were seeded in 6 well plates in triplicates. Cells were cultured in Gln +/- medium for 72h. Cell numbers were quantified with an automated cell counter at the end of the time point. Values represent mean ± SEM, ** P ≤ 0.01, * P ≤ 0.05 (n=3).