Abstract
Immune cells identify and destroy damaged cells to prevent them from causing cancer or other pathologies by mechanisms that remain poorly understood. Here, we report that the cell-cycle inhibitor p21 places cells under immunosurveillance to establish a biological timer mechanism that controls cell fate. p21 activates retinoblastoma protein (Rb)–dependent transcription at select gene promoters to generate a complex bioactive secretome, termed p21-activated secretory phenotype (PASP). The PASP includes the chemokine CXCL14, which promptly attracts macrophages. These macrophages disengage if cells normalize p21 within 4 days, but if p21 induction persists, they polarize toward an M1 phenotype and lymphocytes mount a cytotoxic T cell response to eliminate target cells, including preneoplastic cells. Thus, p21 concurrently induces proliferative arrest and immunosurveillance of cells under duress.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Cycle Checkpoints
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Cell Line
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Cellular Senescence*
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Chemokines, CXC / metabolism
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Cyclin-Dependent Kinase Inhibitor p16 / genetics
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Cyclin-Dependent Kinase Inhibitor p16 / metabolism
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Cyclin-Dependent Kinase Inhibitor p21 / genetics
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism*
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Genes, ras
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Hepatocytes / immunology
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Hepatocytes / metabolism
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Humans
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Immunologic Surveillance*
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Macrophages / immunology
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Macrophages / metabolism
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Mice
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Mice, Transgenic
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Proto-Oncogene Proteins p21(ras) / metabolism
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Retinoblastoma Protein / metabolism
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Stress, Physiological
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T-Lymphocytes, Cytotoxic / immunology
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Transcription, Genetic
Substances
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CXCL14 protein, mouse
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Cdkn1a protein, mouse
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Cdkn2a protein, mouse
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Chemokines, CXC
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Cyclin-Dependent Kinase Inhibitor p16
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Cyclin-Dependent Kinase Inhibitor p21
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Retinoblastoma Protein
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Hras protein, mouse
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Proto-Oncogene Proteins p21(ras)