Next Article in Journal
Linking Cancer Metabolic Dysfunction and Genetic Instability through the Lens of Iron Metabolism
Next Article in Special Issue
PTEN in Lung Cancer: Dealing with the Problem, Building on New Knowledge and Turning the Game Around
Previous Article in Journal
Uveal Melanoma Biopsy: A Review
Previous Article in Special Issue
Phenotype-Driven Diagnostic of PTEN Hamartoma Tumor Syndrome: Macrocephaly, But Neither Height nor Weight Development, Is the Important Trait in Children
Open AccessReview

PTEN Tumor-Suppressor: The Dam of Stemness in Cancer

1
Istituto di Patologia Generale, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
2
Department of Oncology and Molecular Medicine, Istituto Superiore di Sanità, 00161 Rome, Italy
3
Scientific Vice-Direction, Fondazione Policlinico Universitario “A. Gemelli”–I.R.C.C.S., Largo Francesco Vito 1-8, 00168 Rome, Italy
*
Authors to whom correspondence should be addressed.
These authors equally contributed.
Cancers 2019, 11(8), 1076; https://doi.org/10.3390/cancers11081076
Received: 2 July 2019 / Revised: 24 July 2019 / Accepted: 26 July 2019 / Published: 30 July 2019
(This article belongs to the Special Issue PTEN: A Multifaceted Tumor Suppressor)
PTEN is one of the most frequently inactivated tumor suppressor genes in cancer. Loss or variation in PTEN gene/protein levels is commonly observed in a broad spectrum of human cancers, while germline PTEN mutations cause inherited syndromes that lead to increased risk of tumors. PTEN restrains tumorigenesis through different mechanisms ranging from phosphatase-dependent and independent activities, subcellular localization and protein interaction, modulating a broad array of cellular functions including growth, proliferation, survival, DNA repair, and cell motility. The main target of PTEN phosphatase activity is one of the most significant cell growth and pro-survival signaling pathway in cancer: PI3K/AKT/mTOR. Several shreds of evidence shed light on the critical role of PTEN in normal and cancer stem cells (CSCs) homeostasis, with its loss fostering the CSC compartment in both solid and hematologic malignancies. CSCs are responsible for tumor propagation, metastatic spread, resistance to therapy, and relapse. Thus, understanding how alterations of PTEN levels affect CSC hallmarks could be crucial for the development of successful therapeutic approaches. Here, we discuss the most significant findings on PTEN-mediated control of CSC state. We aim to unravel the role of PTEN in the regulation of key mechanisms specific for CSCs, such as self-renewal, quiescence/cell cycle, Epithelial-to-Mesenchymal-Transition (EMT), with a particular focus on PTEN-based therapy resistance mechanisms and their exploitation for novel therapeutic approaches in cancer treatment. View Full-Text
Keywords: cancer stem cells; PTEN; therapy resistance; targeted therapy cancer stem cells; PTEN; therapy resistance; targeted therapy
Show Figures

Figure 1

MDPI and ACS Style

Luongo, F.; Colonna, F.; Calapà, F.; Vitale, S.; Fiori, M.E.; De Maria, R. PTEN Tumor-Suppressor: The Dam of Stemness in Cancer. Cancers 2019, 11, 1076. https://doi.org/10.3390/cancers11081076

AMA Style

Luongo F, Colonna F, Calapà F, Vitale S, Fiori ME, De Maria R. PTEN Tumor-Suppressor: The Dam of Stemness in Cancer. Cancers. 2019; 11(8):1076. https://doi.org/10.3390/cancers11081076

Chicago/Turabian Style

Luongo, Francesca; Colonna, Francesca; Calapà, Federica; Vitale, Sara; Fiori, Micol E.; De Maria, Ruggero. 2019. "PTEN Tumor-Suppressor: The Dam of Stemness in Cancer" Cancers 11, no. 8: 1076. https://doi.org/10.3390/cancers11081076

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
Search more from Scilit
 
Search
Back to TopTop