title: Staphylococcus aureus Enterotoxin B Down-Regulates the Expression of Transforming Growth Factor-Beta (TGF-β) Signaling Transducers in Human Glioblastoma.
abstract: BACKGROUND
  It has been revealed that Staphylococcus aureus enterotoxin B (SEB) may feature anti-cancer and anti-metastatic advantages due to its ability to modify cell immunity processes and signaling pathways. Glioblastoma is one of the most aggressive human cancers; it has a high mortality nature, which makes it an attractive area for the development of novel therapies.
  
  
  OBJECTIVE
  We examined whether the SEB could exert its growth inhibitory effects on glioblastoma cells partially through the manipulation of a key tumor growth factor termed transforming growth factor-beta (TGF-β).
  
  
  METHODS
  A human primary glioblastoma cell line, U87, was treated with different concentrations of SEB. The cell quantity was measured by the MTT assay at different exposure times. For molecular assessments, total ribonucleic acid (RNA) was extracted from either non-treated or SEB-treated cells. Subsequently, the gene expression of TGF-β transducers, smad2/3, at the messenger RNA (mRNA) level, was analyzed via a quantitative real-time polymerase chain reaction (qPCR) using the SYBR Green method. Significant differences between cell viability and gene expression levels were determined (Prism 5.0 software) using one-way analyses of variance (ANOVA) test.
  
  
  RESULTS
  We reported that SEB could effectively down-regulate smad2/3 expression in glioblastoma cells at concentrations as quantity as 1 μg/mL and 2 μg/mL (P < 0.05 and P < 0.01, respectively). The SEB concentrations effective at regulating smad2/3 expression were correlated with those used to inhibit the proliferation of glioblastoma cells. Our results also showed that SEB was able to decrease smad2/3 expression at the mRNA level in a concentration- and time-dependent manner.
  
  
  CONCLUSIONS
  We suggested that SEB could represent an agent that can significantly decrease smad2/3 expression in glioblastoma cells, leading to moderate TGF-β growth signaling and the reduction of tumor cell proliferation.
authors.affiliation: Colorectal Research Center, Iran University of Medical Sciences, Tehran, IR Iran.
authors.forename: Abolfazl
authors.initials: A
authors.lastname: Akbari
authors.affiliation: Department of Medical Mycology, AJA University of Medical Sciences, Tehran, IR Iran.
authors.forename: Zohreh
authors.initials: Z
authors.lastname: Farahnejad
authors.affiliation: Immunogenetic Research Center, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, IR Iran.
authors.forename: Javad
authors.initials: J
authors.lastname: Akhtari
authors.affiliation: Department of Medical Mycology and Parasitology, Invasive Fungi Research Center, School of Medicine, Mazandaran University of Medical Sciences, Sari, IR Iran.
authors.forename: Mahdi
authors.initials: M
authors.lastname: Abastabar
authors.affiliation: Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, IR Iran.
authors.forename: Gholam Reza
authors.initials: GR
authors.lastname: Mobini
authors.affiliation: Department of Medical Mycology, AJA University of Medical Sciences, Tehran, IR Iran.
authors.forename: Amir Seied Ali
authors.initials: AS
authors.lastname: Mehbod
keywords: Cell Signaling Transducers; Glioblastoma; Staphylococcus aureus enterotoxin B; Transforming Growth Factor-β (TGF-β)