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Forum on Immunopathological Diseases and Therapeutics
SJR: 0.164 SNIP: 0.041 CiteScore™: 0.18

ISSN Print: 2151-8017
ISSN Online: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

Forum on Immunopathological Diseases and Therapeutics

DOI: 10.1615/ForumImmunDisTher.v1.i1-2.70
pages 97-114

Yin Yang 1 and raf-1 Kinase Inhibitory Protein Status in Hepatocellular carcinoma: Future Perspectives

Natale D'Alessandro
Pharmacology Unit, University of Palermo Department of Health Sciences and Mother and Child Care "Giuseppe D'Alessandro" Palermo, Italy
Lydia Giannitrapani
Biomedical Department of Internal Medicine and Specialties (DiBiMIS), University of Palermo, Italy
Manuela Labbozzetta
Pharmacology Unit, Department of Health Sciences and Mother and Child Care "G. D'Alessandro", University of Palermo; Palermo, Italy
Paola Poma
Pharmacology Unit, Department of Health Sciences and Mother and Child Care "G. D'Alessandro", University of Palermo; Palermo, Italy
Luigi Inguglia
Department STEBICEF, University of Palermo, Palermo, Italy; Euro Mediterranean Institute of Science and Technology (IEMEST), Palermo, Italy
Ada Maria Florena
Dipartimento di Patologia Umana, Universitü degli Studi di Palermo, Palermo
Rossana Porcasi
Dipartimento di Patologia Umana, Universitü degli Studi di Palermo, Palermo
Melchiorre Cervello
Institute of Biomedicine and Molecular Immunology "Alberto Monroy", National Research Council (CNR) Palermo, Italy
Giuseppe Montalto
Dipartimento di Medicina Clinica e delle Patologie Emergenti, Universitü degli Studi di Palermo, Palermo
Monica Notarbartolo
Pharmacology Unit, Department of Health Sciences and Mother and Child Care "G. D'Alessandro", University of Palermo; Palermo, Italy

ABSTRACT

We focus on to the role of the transcription factors NF-κB and Yin Yang 1 (YY1) and of Raf-1 kinase inhibitory protein (RKIP) in hepatocellular carcinoma (HCC). YY1, whose expression is enhanced by NF-κB, favors tumorigenesis. RKIP inhibits the oncogenic activities of MAPK and NF-κB pathways and promotes drug-induced apoptosis. Mutual influences between YY1 and RKIP may exist and there is separate evidence that relevant increases in YY1 and reductions in RKIP occur in HCC. In a recent study on clinical HCC, we found that, indeed, the ratio of YY1 to RKIP mRNA and protein expression is very frequently profoundly inverted in tumors compared with adjacent tissues. Hyperactivation of YY1 in tumors was corroborated by its nuclear localization and by concomitant increases in the coactivator YY1AP. Overall, the alteration in the YY1-RKIP balance might represent, beside a marker of malignant progression, a target of therapeutic interventions in HCC, which will include application of NF-κB inhibitors, also in conjunction with the active agent sorafenib.