Protein A of Staphylococcus aureus is a pathogenic factor whose encoding gene, spa, shows a variation in length in different strains.
In this study the spa gene variation in S. aureus isolated from healthy carriers and patients was studied, We also compared this variation among MRSA with MSSA strains.
208 strains of Staphylococcus aureus which we were isolated from Gorgan, north of Iran were studied, 121 cases from patients and 87 cases from healthy carriers, 59 out of them were MRSA and 149 MSSA.
Samples DNA were extracted and amplified by specific primer of spa gene.
In 4 (3.8%) strains of them no spa gene was detected, and 10.6% had a dual band (1200 and 1400 bp). In strains with one band, the length of spa gene differed from 1150 to 1500 bp. The most prevalent length was 1350–1400 bp (37%). The frequencies of short spa bands (1150–1200 bp) in patients strains were significantly higher.
In 4 (3.8%) strains of them no spa gene was detected, and 10.6% had a dual band (1200 and 1400 bp). In strains with one band, the length of spa gene differed from 1150 to 1500 bp. The most prevalent length was 1350–1400 bp (37%). The frequencies of short spa bands (1150–1200 bp) in patients strains were significantly higher.
The spa gene length of 1350–1400 bp in MSSA was more than in MRSA strains (P < .05). The average length of spa in isolated strains from urinary tract infections was more than others.
It is concluded that the length of spa gene depends either on resistance to Methicillin or the source of S. aureus isolation.
The cell division cycle 25 (CDC25) phosphatases regulate key transitions between cell-cycle phases during normal cell division, and in the case of DNA damage, they are key targets of the checkpoint machinery that ensure genetic stability. Little is known about the mechanisms underlying dysregulation and downstream targets of CDC25. To understand these mechanisms, we silenced the CDC25A gene in breast cancer cell line MDA-MB-231 and studied downstream targets of CDC25A gene. MDA-MB-231 breast cancer cells were transfected and silenced by CDC25A small interfering RNA. Total messenger RNA (mRNA) was extracted and analyzed by quantitative real-time polymerase chain reaction. CDC25A phosphatase level was visualized by Western blot analysis and was analyzed by 2D electrophoresis and LC-ESI-MS/MS. After CDC25A silencing, cell proliferation reduced, and the expression of 12 proteins changed. These proteins are involved in cell-cycle regulation, programmed cell death, cell differentiation, regulation of gene expression, mRNA editing, protein folding, and cell signaling pathways. Five of these proteins, including ribosomal protein lateral stalk subunit P0, growth factor receptor bound protein 2, pyruvate kinase muscle 2, eukaryotic translation elongation factor 2, and calpain small subunit 1 increase the activity of cyclin D1. Our results suggest that CDC25A controls the cell proliferation and tumorigenesis by a change in expression of proteins involved in cyclin D1 regulation and G1/S transition. K E Y W O R D S breast cancer, CDC25A, cell-cycle, cyclin D1
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