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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN Imprimir: 0893-9675
ISSN En Línea: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.2017020473
pages 49-61

Targeting the Overexpressed YY1 in Cancer Inhibits EMT and Metastasis

Anne Arah Cho
Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, California
Benjamin Bonavida
Department of Microbiology, Immunology, & Molecular Genetics, David Geffen School of Medicine, Johnson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90025-1747


There have been recent developments in the treatment of various cancers, in particular non-metastatic cancers. However, many of the responding patients often relapse initially through the development of spread micro and macro-metastases. Unfortunately, there are very few therapeutic modalities for the treatment of metastatic cancers. The development of cancer metastasis has been proposed to involve the epithelial–mesenchymal transition (EMT), in which the tumor cells with the EMT phenotype exhibit various phenotypic markers and molecular modifications that are manifested to resist most conventional therapies. YY1 is a target of the hyperactivated nuclear factor-kappa beta pathway in cancer and it was reported that YY1 also regulates cell survival and cell proliferation in addition to its role in EMT and resistance. The overexpression of YY1 in the majority of cancers has been correlated with poor prognosis. It is hypothesized that targeting YY1 may result in several anti-tumor activities, including inhibition of cell survival and cell proliferation, inhibition of EMT, and reversal of resistance. This review discusses the potential therapeutic targeting of an overexpressed transcription factor, Yin Yang 1 (YY1), which has been implicated in the development of EMT and drug resistance. Several examples targeting YY1 in experimental models are presented.

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