Y-box Binding Protein-1 Is Part of a Complex Molecular Network Linking ΔNp63α to the PI3K/akt Pathway in Cutaneous Squamous Cell Carcinoma

Cutaneous squamous cell carcinomas (SCCs) typically lack somatic oncogene‐activating mutations and most of them contain p53 mutations. However, the presence of p53 mutations in skin premalignant lesions suggests that these represent early events during tumor progression and additional alterations ma...

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Bibliographic Details
Published in:Journal of cellular physiology 2015-09, Vol.230 (9), p.2067-2074
Main Authors: Troiano, Annaelena, Lomoriello, Irene Schiano, di Martino, Orsola, Fusco, Sabato, Pollice, Alessandra, Vivo, Maria, La Mantia, Girolama, Calabrò, Viola
Format: Article
Language:English
Subjects:
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Cell Line, Tumor
Cell Proliferation - genetics
Cell Survival - genetics
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Humans
Oncogene Protein v-akt - genetics
Oncogene Protein v-akt - metabolism
Phosphatidylinositol 3-Kinases - genetics
Phosphatidylinositol 3-Kinases - metabolism
Signal Transduction - genetics
Skin Neoplasms - genetics
Skin Neoplasms - pathology
Transcription Factors - genetics
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Proteins - genetics
Y-Box-Binding Protein 1 - biosynthesis
Y-Box-Binding Protein 1 - genetics
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Summary:Cutaneous squamous cell carcinomas (SCCs) typically lack somatic oncogene‐activating mutations and most of them contain p53 mutations. However, the presence of p53 mutations in skin premalignant lesions suggests that these represent early events during tumor progression and additional alterations may be required for SCC development. SCC cells frequently express high levels of ΔNp63α and Y‐box binding 1 (YB‐1 or YBX1) oncoproteins. Here, we show that knockdown of YB‐1 in spontaneously immortalized HaCaT and non‐metastatic SCC011 cells led to a dramatic decrease of ΔNp63α, cell detachment and death. In highly metastatic SCC022 cells, instead, YB‐1 silencing induces PI3K/AKT signaling hyperactivation which counteracts the effect of YB‐1 depletion and promotes cell survival. In summary, our results unveil a functional cross‐talk between YB‐1, ΔNp63α and the PI3K/AKT pathway critically governing survival of squamous carcinoma cells. J. Cell. Physiol. 230: 2067–2074, 2015. © 2015 Wiley Periodicals, Inc.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.24934