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• W4361950693 abstract "<div>Abstract<p><b>Purpose:</b> To investigate the clinicopathologic significance, role, and mechanism of action of microRNA-224 (miR-224) in colorectal cancer.</p><p><b>Experimental Design:</b> Real-time PCR was used to quantify miR-224 expression. The association of miR-224 with the clinicopathologic features and survival was evaluated in 110 colorectal cancer patients. The role of miR-224 in colorectal cancer was investigated using <i>in vitro</i> and <i>in vivo</i> assays. Luciferase reporter assays were conducted to confirm target gene associations.</p><p><b>Results:</b> miR-224 was overexpressed in colorectal cancer. High-level expression of miR-224 was significantly associated with an aggressive phenotype and poor prognosis. Overexpression of miR-224 promoted colorectal cancer cell proliferation <i>in vitro</i> and tumor growth <i>in vivo</i>. Specifically, miR-224 accelerated the G₁–S phase transition through activation of AKT/FOXO3a signaling, downregulation of p21Cip1 and p27Kip1, and upregulation of cyclin D1. Moreover, both PH domain leucine-rich-repeats protein phosphatase 1 (<i>PHLPP1</i>) and <i>PHLPP2</i>, antagonists of PI3K/AKT signaling, were confirmed as <i>bona fide</i> targets of miR-224. miR-224 directly targeted the 3′-untranslated regions of the <i>PHLPP1</i> and <i>PHLPP2</i> mRNAs and repressed their expression.</p><p><b>Conclusion:</b> This study reveals functional and mechanistic links between miRNA-224 and the tumor suppressors PHLPP1 and PHLPP2 in the pathogenesis of colorectal cancer. miR-224 not only plays important roles in the regulation of cell proliferation and tumor growth in colorectal cancer, but also has potential as a prognostic marker or therapeutic target for colorectal cancer. <i>Clin Cancer Res; 19(17); 4662–72. ©2013 AACR</i>.</p></div>" @default.
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• W4361950693 date "2023-03-31" @default.
• W4361950693 modified "2023-10-16" @default.
• W4361950693 title "Data from microRNA-224 Promotes Cell Proliferation and Tumor Growth in Human Colorectal Cancer by Repressing <i>PHLPP1</i> and <i>PHLPP2</i>" @default.
• W4361950693 doi "https://doi.org/10.1158/1078-0432.c.6521259.v1" @default.
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