肌醇
下调和上调
PI3K/AKT/mTOR通路
癌细胞
MAPK/ERK通路
生物
癌症
肿瘤进展
癌症研究
蛋白激酶B
细胞生长
调节器
细胞生物学
信号转导
生物化学
受体
遗传学
基因
作者
Kendall C. Case,Michael W. Schmidtke,Miriam L. Greenberg
标识
DOI:10.1007/s10555-022-10032-8
摘要
Inositol is an essential nutrient, obtained either by uptake from the environment or by de novo synthesis from glucose. Inositol and its derivatives exhibit tumor-suppressive effects, potentially mediated by inhibition of the ERK-MAPK or PI3K-Akt pathways. Accordingly, many cancers have been documented to silence expression of the ISYNA1 gene, which encodes the rate-limiting enzyme of inositol synthesis. Paradoxically, recent studies have also reported upregulation of ISYNA1 in some cancers. Upregulation may reflect a compensatory response brought about by defective inositol uptake or oncogenic mutations that preclude its tumor-suppressive effects. In these scenarios, de novo synthesis of inositol may be upregulated to promote cell proliferation. The role of inositol in cancer is further complicated by its ability to inhibit the master metabolic regulator AMPK, which upon activation can either decrease cell proliferation and metastasis or promote cell survival. Due to its potential dual role in cancer, inositol homeostasis must be tightly regulated in tumor cells. Thus, whether inositol acts to suppress or promote tumor progression is determined by the metabolic profile and oncogenic background of the cancer.
科研通智能强力驱动
Strongly Powered by AbleSci AI