Next Article in Journal
NG2 Proteoglycan Enhances Brain Tumor Progression by Promoting Beta-1 Integrin Activation in both Cis and Trans Orientations
Next Article in Special Issue
Timp1 Promotes Cell Survival by Activating the PDK1 Signaling Pathway in Melanoma
Previous Article in Journal / Special Issue
The Role of PI3K Isoforms in Regulating Bone Marrow Microenvironment Signaling Focusing on Acute Myeloid Leukemia and Multiple Myeloma
Review

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

1
Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino 10126, Italy
2
Department of Public Health and Pediatrics, University of Torino, Torino 10126, Italy
*
Author to whom correspondence should be addressed.
These authors equally contributed to this work.
Academic Editor: Marco Falasca
Cancers 2017, 9(4), 30; https://doi.org/10.3390/cancers9040030
Received: 22 February 2017 / Revised: 24 March 2017 / Accepted: 27 March 2017 / Published: 29 March 2017
(This article belongs to the Special Issue PI3K/PDK1/Akt Pathways in Cancer)
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. View Full-Text
Keywords: PI3K; mTOR; proliferation; overgrowth syndrome; polycystic kidney disease PI3K; mTOR; proliferation; overgrowth syndrome; polycystic kidney disease
MDPI and ACS Style

De Santis, M.C.; Sala, V.; Martini, M.; Ferrero, G.B.; Hirsch, E. PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts. Cancers 2017, 9, 30. https://doi.org/10.3390/cancers9040030

AMA Style

De Santis MC, Sala V, Martini M, Ferrero GB, Hirsch E. PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts. Cancers. 2017; 9(4):30. https://doi.org/10.3390/cancers9040030

Chicago/Turabian Style

De Santis, Maria C., Valentina Sala, Miriam Martini, Giovanni B. Ferrero, and Emilio Hirsch. 2017. "PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts" Cancers 9, no. 4: 30. https://doi.org/10.3390/cancers9040030

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop