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Am J Cancer Res. 2015 Mar 15;5(4):1308-18. eCollection 2015.

Mogrol represents a novel leukemia therapeutic, via ERK and STAT3 inhibition.

Author information

1
Beijing University of Agriculture Beijing 102206, China ; National Engineering Laboratory for Industrial Enzymes, Tianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences Tianjin 300308, China ; Key Laboratory of Urban Agriculture (North) of Ministry of Agriculture P. R. China, Beijing University of Agriculture Beijing 102206, China.
2
National Engineering Laboratory for Industrial Enzymes, Tianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences Tianjin 300308, China.
3
Beijing University of Agriculture Beijing 102206, China.
4
Beijing University of Agriculture Beijing 102206, China ; Key Laboratory of Urban Agriculture (North) of Ministry of Agriculture P. R. China, Beijing University of Agriculture Beijing 102206, China.

Abstract

Unlike solid tumors, the primary strategy for leukemia treatment is chemotherapy. However, leukemia chemotherapy is associated with adverse drug effects and drug resistance. Therefore, it is imperative to identify novel agents that effectively treat leukemia while minimizing adverse effects. The Raf/MEK/extracellular regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3) pathways have been implicated in leukemia carcinogenesis, and provide novel molecular targets for therapeutic intervention in cancer. Mogrol, a biometabolite of mogrosides found in Siraitia grosvenorii, has exhibited anti-cancer activities; however, the underlying mechanism of this effect remains unclear. To clarify its anti-cancer activity and mechanism of action, we treated K562 leukemia cells with mogrol. Mogrol suppressed leukemia cell growth via inhibition of the ERK1/2 and STAT3 pathways, in particular, through the suppression of p-ERK1/2 and p-STAT3. Inhibition of these pathways suppressed Bcl-2 expression, thereby inducing K562 cell apoptosis. Furthermore, mogrol enhanced p21 expression, resulting in G0/G1 cell cycle arrest. The findings provide new perspectives regarding the role of mogrol in leukemia treatment.

KEYWORDS:

ERK1/2; Mogrosides; STAT3; apoptosis; mogrol

PMID:
26101699
PMCID:
PMC4473312

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