Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors

被引：22

作者：

Csibi, Alfredo ^{[1
]}

Blenis, John ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

来源：

BMC BIOLOGY | 2011年 / 9卷

关键词：

CELL-GROWTH; LYMPHANGIOLEIOMYOMATOSIS;

D O I：

10.1186/1741-7007-9-69

中图分类号：

Q [生物科学];

学科分类号：

090105 [作物生产系统与生态工程];

摘要：

The elevated metabolic requirements of cancer cells reflect their rapid growth and proliferation and are met through mutations in oncogenes and tumor suppressor genes that reprogram cellular processes. For example, in tuberous sclerosis complex (TSC)-related tumors, the loss of TSC1/2 function causes constitutive mTORC1 activity, which stimulates glycolysis, resulting in glucose addiction in vitro. In research published in Cell and Bioscience, Jiang and colleagues show that pharmacological restriction of glucose metabolism decreases tumor progression in a TSC xenograft model.

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页数：5

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