癌症中心碳代谢
中文名称
通路描述
细胞恶性转化需要特定的细胞代谢适应以支持生长和生存。在 20 世纪初,奥托·瓦格纳建立了恶性组织中中央代谢途径存在根本差异的事实。他表明癌细胞消耗大量葡萄糖,维持高糖酵解速率并将大部分葡萄糖转化为乳酸,即使在正常氧气浓度下(瓦格纳效应)。最近,人们认识到'瓦格纳效应'还包括类似增加的谷氨酰胺利用。从增强糖酵解和谷氨酰胺分解提供的中间分子中,癌细胞合成大多数用于其生物量和基因组复制的大分子所需的大分子。这些癌症特异性改变是遗传突变和癌症细胞中信号通路变化的主要后果。三个转录因子 c-MYC、HIF-1 和 p53 是关键调节者,以不同方式协调癌症代谢,许多其他原癌基因和肿瘤抑制基因沿调节 c-MYC、HIF-1 和 p53 的信号通路聚集。
英文描述
Malignant transformation of cells requires specific adaptations of cellular metabolism to support growth and survival. In the early twentieth century, Otto Warburg established that there are fundamental differences in the central metabolic pathways operating in malignant tissue. He showed that cancer cells consume a large amount of glucose, maintain high rate of glycolysis and convert a majority of glucose into lactic acid even under normal oxygen concentrations (Warburg's Effects). More recently, it has been recognized that the 'Warburg effect' encompasses a similarly increased utilization of glutamine. From the intermediate molecules provided by enhanced glycolysis and glutaminolysis, cancer cells synthesize most of the macromolecules required for the duplication of their biomass and genome. These cancer-specific alterations represent a major consequence of genetic mutations and the ensuing changes of signalling pathways in cancer cells. Three transcription factors, c-MYC, HIF-1 and p53, are key regulators and coordinate regulation of cancer metabolism in different ways, and many other oncogenes and tumor suppressor genes cluster along the signaling pathways that regulate c-MYC, HIF-1 and p53.
所含基因
71 个基因
AKT1
AKT2
AKT3
EGFR
ERBB2
FGFR1
FGFR2
FGFR3
FLT3
G6PD
GCK
GLS
GLS2
HIF1A
HK1
HK2
HK3
HKDC1
HRAS
IDH1
IDH2
KIT
KRAS
LDHA
LDHAL6A
LDHAL6B
LDHB
LDHC
MAP2K1
MAP2K2
MAPK1
MAPK3
MET
MTOR
MYC
NRAS
NTRK1
NTRK3
P3R3URF-PIK3R3
PDGFRA
PDGFRB
PDHA1
PDHA2
PDHB
PDK1
PFKL
PFKM
PFKP
PGAM1
PGAM2
PGAM4
PIK3CA
PIK3CB
PIK3CD
PIK3R1
PIK3R2
PIK3R3
PKM
PTEN
RAF1
RET
SCO2
SIRT3
SIRT6
SLC16A3
SLC1A5
SLC2A1
SLC2A2
SLC7A5
TIGAR
TP53