Abstract
Energy metabolism in cancer cells is often increased to meet their higher proliferative rate and biosynthesis demands. Suppressing cancer cell metabolism using agents like metformin has become an attractive strategy for treating cancer patients. We showed that a novel ginsenoside derivative, Rh2E2, is as effective as aspirin in preventing the development of AOM/DSS-induced colorectal cancer and suppresses tumor growth and metastasis in a LLC-1 xenograft. A sub-chronic and acute toxicity LD50 test of Rh2E2 showed no harmful reactions at the maximum oral dosage of 5000 mg/kg body weight in mice. Proteomic profiling revealed that Rh2E2 specifically inhibited ATP production in cancer cells via down-regulation of metabolic enzymes involving glycolysis, fatty acid β-oxidation and the tricarboxylic acid cycle, leading to specific cytotoxicity and S-phase cell cycle arrest in cancer cells. Those findings suggest that Rh2E2 possesses a novel and safe anti-metabolic agent for cancer patients by specific reduction of energy-based metabolism in cancer cells.
Highlights
18F-deoxyglucose positron emission tomography (FDG-PET) is often used to visualize the increased glucose uptake in tumors of patients [1]
We showed that a novel ginsenoside derivative, Rh2E2, is as effective as aspirin in preventing the development of AOM/dextran sodium sulfate (DSS)-induced colorectal cancer and suppresses tumor growth and metastasis in a LLC-1 xenograft
The hydroxyl group located at C-20 of these epoxides attacked the electron-demand C-24 to form 20, 24-epoxides in a 1:1 mixture of 24-epimers [22], which was validated by UPLC-MS analysis and purified by ODS column chromatography (90% methanol)
Summary
18F-deoxyglucose positron emission tomography (FDG-PET) is often used to visualize the increased glucose uptake in tumors of patients [1]. The proliferating cancer cells exhibit a higher cell metabolism compared to most normal differentiated cells [2]. To adapt to the higher rate of proliferation and division of cancer cells, demand of the additional nutrients and sufficient energy are required [3]. Studies of metabolic alteration and adaptation of cancer cells over the past century [4] revealed that glycolysis and glutaminolysis are the major enhanced metabolic pathways for tumor growth and survival [5]. Inhibiting multiple mechanisms to reduce or reverse the abnormal reprogrammed metabolism of cancer cells, reducing energy-based metabolism, is an attractive therapeutic strategy for cancer patients [3]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
