Extrinsic versus intrinsic activation of p16INK4a.

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miR-133a positively regulated p53/p21 pathway.

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Extrinsic versus intrinsic activation of p16INK4a. Extrinsic versus intrinsic activation of p16INK4a. A, injection of Lkb1-null endometrial cancer cells into a syngenic mouse heterozygous for the p16LUC reporter causes stromal luciferase expression upon tumor growth. Injection of Matrigel vehicle on the opposite flank does not alter p16INK4a expression. (See also ref. 130.) B, intrinsic signals induces p16INK4a expression in damaged, senescent, or transformed cells. Alterations in surrounding the cellular milieu can trigger the induction of p16INK4a in nearby undamaged cells through an unknown pathway. Kyle M. LaPak, and Christin E. Burd Mol Cancer Res 2014;12:167-183 ©2014 by American Association for Cancer Research