Experimental study on the therapeutic effect and underlining mechanisms of positron in pancreatic cancer cells
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Ying Wang1,2, Ming Li3, Rao Diao1, Brian Tung2, Dalong Zhang1 and Yaming Li1
1Department of Nuclear Medicine, First Affiliated Hospital of China Medical University, Shenyang, Liaoning, China
2Department of Radiology, Massachusetts General Hospital, Boston, Massachusetts, USA
3Department of Urology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China
Yaming Li, email: email@example.com
Keywords: pancreatic cancer, apoptosis, positron, 18F-FDG, microPET
Received: March 14, 2017 Accepted: May 03, 2017 Published: June 05, 2017
The purpose of this study was to assess the potential therapeutic effect of positrons emitted by 18F-2-Deoxy-2-Fluoro-D-Glucose (18F-FDG) on pancreatic cancer cells and elucidate its underlying mechanisms. Pancreatic cancer cells were incubated with different radioactive concentrations of 18F-FDG and evaluated for anti-cancer properties and underlining mechanisms. In addition, three groups of tumor-bearing mice were treated with different doses of 18F-FDG weekly, the tumor growth rate was calculated, and the mice were imaged by positron emission tomography (PET) with 18F-FDG before and after treatment. The presence of apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) stain and immunohistochemistry analysis. All treated groups exhibited positron-inhibited proliferation and positron-induced apoptosis compared with the control group in vitro. Further, we noted that higher treatment dose correlated with a better treatment response. In vivo, the high dose administration of 18F-FDG reduced tumor growth and prolonged the survival of treated mice compared with the control group with no change in the behavior or normal tissues of the mice. Immunohistochemical analysis and TUNEL stain showed more apoptotic cells than that in control group. The results demonstrated that positron radiation inhibited the proliferation and induced apoptosis of pancreatic cancer cells in vitro and in vivo, via an endogenous mitochondria-mediated signaling pathway.
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