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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2.2

ISSN 印刷: 0893-9675
ISSN オンライン: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.2017020836
pages 23-36

Yin Yang 1 (YY1): Regulation of Survivin and Its Role In Invasion and Metastasis

Nicholas R. Galloway
Department of Basic Science and Division of Biochemistry, Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, California 92350
Kathryn F. Ball
Department of Basic Science and Division of Biochemistry, Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, California 92350
TessaRae Stiff
Department of Basic Science and Division of Biochemistry, Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, California 92350
Nathan R. Wall
Department of Basic Science and Division of Biochemistry, Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, California 92350

要約

Despite significant clinical and basic science advancements, cancer remains a devastating disease that affects people of all ages, races, and backgrounds. The pathogenesis of cancer has recently been described to result from eight biological capabilities or hallmarks and two enabling characteristics. These eight hallmarks are: deregulation of cellular energetics, avoiding immune destruction, enabling replicative immortality, inducing angiogenesis, sustaining proliferative signaling, evading growth suppressors, resisting cell death, and activating invasion and metastasis. The enabling characteristics are: genome instability and mutation and tumor-promoting inflammation. Survivin, the fourth most common transcript found in cancer cells, is a protein that is thought to be involved in the enhanced proliferation, survival, and metastasis and possibly other key hallmarks of cancer cells. Understanding how this gene is turned on and off is vitally important for attempt improving cancer management and therapy. Our work has identified a novel transcriptional regulator of survivin called Yin Yang 1 (YY1), which has been observed to activate some gene promoters and repress others and is gaining increasing interest as a target of cancer therapy. Our work shows for the first time that YY1 represses survivin transcription by physically interacting with the survivin promoter. Furthermore, YY1 appears to contribute to basal survivin transcriptional activity, indicating that disruption of its binding may in part contribute to survivin overexpression after cellular stress events including chemotherapy and radiotherapy.


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