title: Decoy-DNA against special AT-rich sequence binding protein 1 inhibits the growth and invasive ability of human breast cancer.
abstract: "Triple-negative" (TN) breast cancers, which are characterized by estrogen receptor (-), progesterone receptor (-), and human epidermal growth factor receptor 2 (-), are typically associated with poor prognosis because of their aggressive tumor phenotypes. In recent years, the number of patients with breast cancers has remarkably increased, but there are only few available drugs for treatment of TN breast cancers. The development of novel drugs targeting TN breast cancer is urgently required. In the present study, we focused on the function of special AT-rich sequence binding protein 1 (SATB1) as a target molecule for the treatment of TN breast cancers. By recruiting chromatin remodeling enzymes and transcriptional factors, SATB1 regulates the expression of >1,000 genes related to cell growth and translocation. We synthesized a decoy DNA against SATB1, including the recognition sequence of SATB1. We examined the inhibitory effects of the decoy DNAs on cellular proliferation of a TN metastatic breast cancer cell line (MDA-MB-231). SATB1-decoy DNA inhibited the proliferation of MDA-MB-231 cells. Especially, it was significant that SATB1-decoy DNA drastically reduced the invasive and metastatic capacity of MBA-MB-231 cells. Further, in the case of MCF7 cells (SATB1-negative breast cancer cell line), SATB1-decoy DNA did not exhibit any inhibitory effect. These data suggest that SATB1-decoy DNA may be an effective candidate for use as a molecular-targeting drug for treatment of TN breast cancer.
authors.affiliation: Department of Biomolecular Engineering, Kyoto Institute of Technology , Matsugasaki, Kyoto, Japan. asakoy@kit.ac.jp
authors.forename: Asako
authors.initials: A
authors.lastname: Yamayoshi
authors.forename: Mariko
authors.initials: M
authors.lastname: Yasuhara
authors.forename: Sanjeev
authors.initials: S
authors.lastname: Galande
authors.forename: Akio
authors.initials: A
authors.lastname: Kobori
authors.forename: Akira
authors.initials: A
authors.lastname: Murakami
mesh_terms: D001943:Breast Neoplasms / Q000235:genetics / Q000473:pathology* / Q000628:therapy*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D055513:Connective Tissue Growth Factor / Q000187:drug effects / Q000378:metabolism; D004247:DNA / Q000138:chemical synthesis / Q000235:genetics / Q000494:pharmacology; D004268:DNA-Binding Proteins / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D005260:Female; D015316:Genetic Therapy; D006801:Humans; D036961:Matrix Attachment Region Binding Proteins / Q000037:antagonists & inhibitors* / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D009361:Neoplasm Invasiveness / Q000235:genetics; D009841:Oligonucleotides / Q000138:chemical synthesis / Q000235:genetics / Q000494:pharmacology*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000187:drug effects / Q000378:metabolism; D000071999:S100 Calcium-Binding Protein A4; D009418:S100 Proteins / Q000187:drug effects / Q000378:metabolism; D042561:Vascular Endothelial Growth Factor B / Q000187:drug effects / Q000378:metabolism
chemical_list: D055513:Connective Tissue Growth Factor; D004247:DNA; D004268:DNA-Binding Proteins; D036961:Matrix Attachment Region Binding Proteins; D009841:Oligonucleotides; D018719:Erb-b2 Receptor Tyrosine Kinases; D000071999:S100 Calcium-Binding Protein A4; D009418:S100 Proteins; D042561:Vascular Endothelial Growth Factor B; C526317:CCN2 protein, human; C076189:SATB1 protein, human; C077591:S100A4 protein, human; C508053:ERBB2 protein, human