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• W2180346476 abstract "Abstract Cancer stem–like cells (CSC) have been proposed to promote cancer progression by initiating tumor growth at distant sites, suggesting that stem-like cell features can support metastatic efficiency. Here, we demonstrate that oncogenic DNp73, a dominant-negative variant of the tumor-suppressor p73, confers cancer cells with enhanced stem-like properties. DNp73 overexpression in noninvasive melanoma and lung cancer cells increased anchorage-independent growth and elevated the expression of the pluripotency factors CD133, Nanog, and Oct4. Conversely, DNp73 depletion in metastatic cells downregulated stemness genes, attenuated sphere formation and reduced the tumor-initiating capability of spheroids in tumor xenograft models. Mechanistic investigations indicated that DNp73 acted by attenuating expression of miR-885-5p, a direct regulator of the IGF1 receptor (IGF1R) responsible for stemness marker expression. Modulating this pathway was sufficient to enhance chemosensitivity, overcoming DNp73-mediated drug resistance. Clinically, we established a correlation between low p73 function and high IGF1R/CD133/Nanog/Oct4 levels in melanoma specimens that associated with reduced patient survival. Our work shows how DNp73 promotes cancer stem–like features and provides a mechanistic rationale to target the DNp73–IGF1R cascade as a therapeutic strategy to eradicate CSC. Cancer Res; 76(2); 197–205. ©2015 AACR." @default.
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• W2180346476 date "2016-01-14" @default.
• W2180346476 modified "2023-10-13" @default.
• W2180346476 title "p73 and IGF1R Regulate Emergence of Aggressive Cancer Stem–like Features via miR-885-5p Control" @default.
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• W2180346476 doi "https://doi.org/10.1158/0008-5472.can-15-1228" @default.
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