title: gef gene expression in MCF-7 breast cancer cells is associated with a better prognosis and induction of apoptosis by p53-mediated signaling pathway.
abstract: Breast cancer research has developed rapidly in the past few decades, leading to longer survival times for patients and opening up the possibility of developing curative treatments for advanced breast cancer. Our increasing knowledge of the biological pathways associated with the progression and development of breast cancer, alongside the failure of conventional treatments, has prompted us to explore gene therapy as an alternative therapeutic strategy. We previously reported that gef gene from E. coli has shown considerable cytotoxic effects in breast cancer cells. However, its action mechanism has not been elucidated. Indirect immunofluorescence technique using flow cytometry and immunocytochemical analysis were used to detect breast cancer markers: estrogen (ER) and progesterone (PR) hormonal receptors, human epidermal growth factor receptor-2 proto-oncogene (c-erbB-2), ki-67 antigen and p53 protein. gef gene induces an increase in ER and PR expressions and a decrease in ki-67 and c-erbB-2 gene expressions, indicating a better prognosis and response to treatment and a longer disease-free interval and survival. It also increased p53 expression, suggesting that gef-induced apoptosis is regulated by a p53-mediated signaling pathway. These findings support the hypothesis that the gef gene offers a new approach to gene therapy in breast cancer.
authors.affiliation: Basic Cardiovascular Research Section, Department of Anatomy and Human Embriology, School of Medicine, University of Granada, Granada E-18012, Spain; E-Mails:  pablo.alvarez.ext@juntadeandalucia.es  (P.J.A.);  jcpradois@ugr.es  (J.P.);  marchal@ugr.es  (J.M.);  cmelguizo@ugr.es  (C.M.);  esmeralda@ugr.es  (E.C.);  fernr@ugr.es  (F.R.).
authors.forename: Houria
authors.initials: H
authors.lastname: Boulaiz
authors.forename: Pablo J
authors.initials: PJ
authors.lastname: Alvarez
authors.forename: Jose
authors.initials: J
authors.lastname: Prados
authors.forename: Juan
authors.initials: J
authors.lastname: Marchal
authors.forename: Consolación
authors.initials: C
authors.lastname: Melguizo
authors.forename: Esmeralda
authors.initials: E
authors.lastname: Carrillo
authors.forename: Macarena
authors.initials: M
authors.lastname: Peran
authors.forename: Fernando
authors.initials: F
authors.lastname: Rodríguez
authors.forename: Alberto
authors.initials: A
authors.lastname: Ramírez
authors.forename: Raúl
authors.initials: R
authors.lastname: Ortíz
authors.forename: Antonia
authors.initials: A
authors.lastname: Aránega
mesh_terms: D017209:Apoptosis / Q000235:genetics*; D001943:Breast Neoplasms / Q000175:diagnosis* / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005819:Genetic Markers; D015316:Genetic Therapy; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000235:genetics / Q000378:metabolism; D061986:MCF-7 Cells; D011379:Prognosis; D000090063:Proto-Oncogene Mas; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics / Q000378:metabolism; D011960:Receptors, Estrogen / Q000235:genetics / Q000378:metabolism; D011980:Receptors, Progesterone / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
chemical_list: D004268:DNA-Binding Proteins; D005819:Genetic Markers; D019394:Ki-67 Antigen; D000090063:Proto-Oncogene Mas; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; C000715470:MAS1 protein, human; C480633:SLC2A4RG protein, human; C495901:TP53 protein, human; C508053:ERBB2 protein, human