Epigenetic changes and nuclear factor-κB activation, but not microRNA-224, downregulate Raf-1 kinase inhibitor protein in triple-negative breast cancer SUM 159 cells

Oncology Letters
Manuela LabbozzettaMonica Notarbartolo

Abstract

Raf-1 kinase inhibitor protein (RKIP) is a tumor suppressor and metastasis inhibitor, which enhances drug-induced apoptosis of cancer cells. Downregulation of RKIP may be significant in the biology of highly aggressive and drug-resistant tumors, for example triple-negative breast cancers (TNBCs). Potential causes for the low levels of RKIP expressed by SUM 159 TNBC cells were investigated in the present study. Bisulphite modification, methylation specific-polymerase chain reaction (PCR) and a TransAM NF-κB assay were performed and the results suggested that various mechanisms, including methylation of the gene promoter, histone deacetylation and nuclear factor-κB (NF-κB) activation, but not targeting by microRNA-224 (miR/miRNA-224), as determined by transfection of pre-miR-224 miRNA precursor or anti-miR-224 miRNA inhibitor, may downregulate RKIP in these cells. Furthermore, reverse transcription-quantitative PCR, western blotting, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium cell growth assay and flow cytometry revealed that in SUM 159 cells, the demethylating agent 5-aza-2'-deoxycytidine (5-AZA), the histone deacetylase inhibitor trichostatin A (TSA) and the NF-κB inhibitor dehydro...Continue Reading

References

Apr 19, 2007·American Journal of Clinical Pathology·Parham MinooAlessandro Lugli
Dec 19, 2007·Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology·Ada Maria FlorenaVito Franco
Nov 4, 2009·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Marilena V Iorio, Carlo M Croce
Oct 6, 2010·Advances in Genetics·Muller Fabbri, George A Calin
Feb 22, 2011·Omics : a Journal of Integrative Biology·Monica NotarbartoloNatale D'Alessandro
Jul 5, 2011·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·K Umezawa
Oct 11, 2011·Forum on Immunopathological Diseases and Therapeutics·Evan J WalkerMiran Kim
Dec 20, 2011·Journal of Cancer Research and Clinical Oncology·Feng-Xian ZhaiDong-Jun Lin
Mar 1, 2012·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Chunfang HaoZhi-hua Zhu
Jul 20, 2012·Biochemical and Biophysical Research Communications·Lin HuangXi Wang
Jul 28, 2012·Journal of Mammary Gland Biology and Neoplasia·Roisin Connolly, Vered Stearns
Oct 26, 2012·Omics : a Journal of Integrative Biology·Paola PomaMonica Notarbartolo
Sep 6, 2013·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·Tun-Chieh ChenYen-Hsu Chen
Mar 13, 2014·American Journal of Clinical Pathology·Robert SchmadekaMeenakshi Singh
Jul 22, 2014·Cancer·Vandana G AbramsonJennifer A Pietenpol

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Citations

Apr 8, 2017·Omics : a Journal of Integrative Biology·Paola PomaMonica Notarbartolo
Sep 6, 2018·Cancers·Ali Ekrem Yesilkanal, Marsha Rich Rosner
Feb 9, 2017·Oncotarget·Esperanza Martín-SánchezDavid Guerrero-Setas
May 1, 2020·International Journal of Molecular Sciences·Manuela LabbozzettaPaola Poma

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