共 103 条
Metformin as an Anticancer Agent
被引:208
作者:

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Bu, Pengli
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St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA

Bhagwat, Madhura
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St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA

Zeng, Joey
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St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA

Vancurova, Ivana
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St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA
机构:
[1] St Johns Univ, Dept Biol Sci, Queens, NY 11439 USA
关键词:
ACTIVATED PROTEIN-KINASE;
AMINO-ACID LEVELS;
BREAST-CANCER;
RAG GTPASES;
PROSTATE-CANCER;
OPPORTUNITY NEOADJUVANT;
HEPATIC GLUCONEOGENESIS;
CELL-PROLIFERATION;
GLUCOSE-PRODUCTION;
CARBON METABOLISM;
D O I:
10.1016/j.tips.2018.07.006
中图分类号:
R9 [药学];
学科分类号:
1007 ;
摘要:
Metformin has been a frontline therapy for type 2 diabetes (T2D) for many years. Its effectiveness in T2D treatment is mostly attributed to its suppression of hepatic gluconeogenesis; however, the mechanistic aspects of metformin action remain elusive. In addition to its glucose-lowering effect, metformin possesses other pleiotropic health-promoting effects that include reduced cancer risk and tumorigenesis. Metformin inhibits the electron transport chain (ETC) and ATP synthesis; however, recent data reveal that metformin regulates AMP-activated protein kinase (AMPK) and the mechanistic target of rapamycin complex 1 (mTORC1) by multiple, mutually nonexclusive mechanisms that do not necessarily depend on the inhibition of ETC and the cellular ATP level. In this review, we discuss recent advances in elucidating the molecular mechanisms that are relevant for metformin use in cancer treatment.
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页码:867 / 878
页数:12
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