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Modulation of Transforming Growth Factor-Β Signalling Transducers in Colon Adenocarcinoma Cells Induced by Staphylococcal Enterotoxin B Publisher Pubmed



Akbari A1 ; Reza Mobini G2 ; Maghsoudi R3 ; Akhtari J4 ; Faghihloo E5 ; Farahnejad Z6, 7
Authors
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Authors Affiliations
  1. 1. Colorectal Research Center, Iran University of Medical Sciences, Tehran, 1313114456, Iran
  2. 2. Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, 8815713471, Iran
  3. 3. Department of Microbiology and Immunology, Shahrekord University of Medical Sciences, Shahrekord, 8815713471, Iran
  4. 4. Immunogenetic Research Center, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, 48175866, Iran
  5. 5. Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, 1313114456, Iran
  6. 6. Department of Medical Mycology, AJA University of Medical Sciences, West Fatemi Avenue, Tehran, 1917793164, Iran
  7. 7. Department of Microbiology, Infectious Diseases Research Center, AJA University of Medical Sciences, Tehran, 1917793164, Iran

Source: Molecular Medicine Reports Published:2016


Abstract

Colorectal cancer (CRC) is a notable cause of cancer-associated mortality worldwide, making it a pertinent topic for the study of cancer and its treatment. Staphylococcal enterotoxin B (SEB), an enterotoxin produced by Staphylococcus aureus, has been demonstrated to exert anticancer and antimetastatic effects due to its ability to modify cell immunity and cellular signaling pathways. In the current study, SEB was investigated, including whether it exerts its growth inhibitory effects on colon adenocarcinoma cells. This may occur through the manipulation of a key tumor growth factor, termed transforming growth factor-β (TGF-β), and its signaling pathway transducer, Smad2/3. The human colon adenocarcinoma HCT116 cell line was treated with different concentrations of SEB, and cell number was measured using MTT assay at different treatment times. Smad2/3 RNA expression level was analyzed in untreated or SEB-treated cells using quantitative polymerase chain reaction, which indicated significant differences between cell viability and Smad2/3 expression levels. SEB effectively downregulated Smad2/3 expression in the HCT116 cells at concentrations of 1 and 2 μg/ml (P=0.0021 and P=0.0017, respectively). SEB concentrations that were effective at inhibiting Smad2/3 expression were correlated with those able to inhibit the proliferation of the cancer cells. SEB inhibited Smad2/3 expression at the mRNA level in a concentration- and time-dependent manner. The present study thus proposed SEB as an agent able to significantly reduce Smad2/3 expression in colon cancer cells, provoking moderate TGF-β growth signaling and the reduction of tumor cell proliferation.