miRNAs link metabolic reprogramming to oncogenesis

被引：78
作者：
Hatziapostolou, Maria
Polytarchou, Christos
Iliopoulos, Dimitrios [1 ]
机构：
[1] Univ Calif Los Angeles, Ctr Syst Biomed, Div Digest Dis, Los Angeles, CA 90095 USA
来源：
TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2013年 / 24卷 / 07期
关键词：
miRNAs; metabolism; cancer; therapy; SQUAMOUS-CELL CARCINOMA; MICRORNA EXPRESSION PROFILES; TARGETING CANCER METABOLISM; TUMOR-SUPPRESSOR P53; HUMAN GASTRIC-CANCER; KINASE TYPE M2; DOWN-REGULATION; C-MYC; PYRUVATE-KINASE; GENE-EXPRESSION;
D O I：
10.1016/j.tem.2013.03.002
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
The most profound biochemical phenotype of cancer cells is their ability to metabolize glucose to lactate, even under aerobic conditions. This alternative metabolic circuitry is sufficient to support the biosynthetic and energy requirements for cancer cell proliferation and metastasis. Alterations in oncogenes and tumor-suppressor genes are involved in the metabolic switch of cancer cells to aerobic glycolysis, increased glutaminolysis, and fatty acid biosynthesis. miRNAs mediate fine-tuning of genes involved directly or indirectly in cancer metabolism. In this review we discuss the regulatory role of miRNAs on enzymes, signaling pathways, and transcription factors involved in glucose and lipid metabolism. We further consider the therapeutic potential of metabolism-related miRNAs in cancer.
引用
收藏
页码：361 / 373
页数：13
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