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Y‐box Binding Protein‐1 Is Part of a Complex Molecular Network Linking ΔNp63α to the PI3K/akt Pathway in Cutaneous Squamous Cell Carcinoma
Author(s) -
Troiano Annaelena,
Lomoriello Irene Schiano,
di Martino Orsola,
Fusco Sabato,
Pollice Alessandra,
Vivo Maria,
La Mantia Girolama,
Calabrò Viola
Publication year - 2015
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24934
Subject(s) - hacat , protein kinase b , cancer research , gene silencing , pi3k/akt/mtor pathway , cell , biology , gene knockdown , cell culture , signal transduction , microbiology and biotechnology , genetics , gene
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.