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Int. J. Mol. Sci. 2016, 17(1), 89; doi:10.3390/ijms17010089

Survivin Modulates Squamous Cell Carcinoma-Derived Stem-Like Cell Proliferation, Viability and Tumor Formation in Vivo

1
Laboratory of Cutaneous Biology, Department of Surgical, Medical, Dental and Morphological Sciences, University of Modena and Reggio Emilia, via del Pozzo 71, 41124 Modena, Italy
2
Ospedale Civile di Sassuolo, Via Francesco Ruini 2, 41049 Sassuolo (MO), Italy
3
Department of Laboratories and Pathologic Anatomy, University of Modena and Reggio Emilia, Via del Pozzo 71, 41124 Modena, Italy
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Wilhelm Volch
Received: 2 December 2015 / Revised: 22 December 2015 / Accepted: 31 December 2015 / Published: 12 January 2016
(This article belongs to the Special Issue Stem Cell Activation in Adult Organism)
View Full-Text   |   Download PDF [2475 KB, uploaded 26 January 2016]   |  

Abstract

Squamous Cell Carcinoma-derived Stem-like Cells (SCC-SC) originate from alterations in keratinocyte stem cells (KSC) gene expression and sustain tumor development, invasion and recurrence. Since survivin, a KSC marker, is highly expressed in SCC-SC, we evaluate its role in SCC-SC cell growth and SCC models. Survivin silencing by siRNA decreases clonal growth of SCC keratinocytes and viability of total, rapidly adhering (RAD) and non-RAD (NRAD) cells from primary SCC. Similarly, survivin silencing reduces the expression of stem cell markers (OCT4, NOTCH1, CD133, β1-integrin), while it increases the level of differentiation markers (K10, involucrin). Moreover, survivin silencing improves the malignant phenotype of SCC 3D-reconstruct, as demonstrated by reduced epidermal thickness, lower Ki-67 positive cell number, and decreased expression of MMP9 and psoriasin. Furthermore, survivin depletion by siRNA in RasG12V-IκBα-derived tumors leads to smaller tumor formation characterized by lower mitotic index and reduced expression of the tumor-associated marker HIF1α, VEGF and CD51. Therefore, our results indicate survivin as a key gene in regulating SCC cancer stem cell formation and cSCC development. View Full-Text
Keywords: squamous cell carcinoma; stem cells; β1-integrin; tumor formation; survivin; rapidly adhering cells; skin; tumorigenesis; differentiation squamous cell carcinoma; stem cells; β1-integrin; tumor formation; survivin; rapidly adhering cells; skin; tumorigenesis; differentiation
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Lotti, R.; Palazzo, E.; Petrachi, T.; Dallaglio, K.; Saltari, A.; Truzzi, F.; Quadri, M.; Puviani, M.; Maiorana, A.; Marconi, A.; Pincelli, C. Survivin Modulates Squamous Cell Carcinoma-Derived Stem-Like Cell Proliferation, Viability and Tumor Formation in Vivo. Int. J. Mol. Sci. 2016, 17, 89.

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