PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts

被引：38

作者：

De Santis, Maria Chiara ^{[1
]}

Sala, Valentina ^{[1
]}

Martini, Miriam ^{[1
]}

Ferrero, Giovanni Battista ^{[2
]}

Hirsch, Emilio ^{[1
]}

机构：

[1] Univ Torino, Dept Mol Biotechnol & Hlth Sci, I-10126 Turin, Italy

[2] Univ Torino, Dept Publ Hlth & Pediat, I-10126 Turin, Italy

来源：

CANCERS | 2017年 / 9卷 / 04期

关键词：

PI3K; mTOR; proliferation; overgrowth syndrome; polycystic kidney disease; TUBEROUS SCLEROSIS COMPLEX; HAMARTOMA TUMOR SYNDROME; PHOSPHOINOSITIDE; 3-KINASES; PIK3CA(H1047R) MUTATION; ACTIVATING MUTATIONS; ONCOGENIC MUTATIONS; CLOVES SYNDROME; EPIDERMAL-NEVI; PIK3CA CAUSE; DISEASE;

D O I：

10.3390/cancers9040030

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The members of the PhosphoInositide-3 Kinase (PI3K) protein family are well-known regulators of proliferative signals. By the generation of lipid second messengers, they mediate the activation of AKT/PKB (AKT) and mammalian Target Of Rapamycin (mTOR) pathways. Although mutations in the PI3K/AKT/mTOR pathway are highly characterized in cancer, recent evidence indicates that alterations in the proliferative signals are major drivers of other diseases such as overgrowth disorders and polycystic kidney disease. In this review, we briefly summarize the role of the PI3K/AKT/mTOR pathway in cell proliferation by comparing the effect of alterations in PI3K enzymes in different tissues. In particular, we discuss the most recent findings on how the same pathway may lead to different biological effects, due to the convergence and cooperation of different signaling cascades.

引用

页数：11

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