Rh2E2, a novel metabolic suppressor, specifically inhibits energy-based metabolism of tumor cells

Vincent Kam Wai Wong, Hang Dong, Xu Liang, Li Ping Bai, Zhi Hong JIANG, Yue Guo, Ah Ng Tony Kong, Rui Wang, Richard Kin Ting Kam, Betty Yuen Kwan Law, Wendy W L HSIAO, Ka Man Chan, Jingrong Wang, Rick Wai Kit Chan, Jianru Guo, Wei Zhang, Feng Gen Yen, Hua Zhou, Elaine Lai Han Leung, Zhiling YULiang LIU*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)9907-9924
Number of pages18
JournalOncotarget
Volume7
Issue number9
DOIs
Publication statusPublished - 2016

Scopus Subject Areas

  • Oncology

User-Defined Keywords

  • Alpha-enolase
  • Anti-tumor
  • Energy metabolism
  • Metabolic suppressor
  • Rh2E2

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