Abstract
The crucial role of phospholipase C epsilon (PLC e) in cancinogensis has been described recently. However, whether or not it decreases the methyl-nitroso-urea (MNU) induced rats’ bladder tumorigenesis and the probable mechanism remains poorly understood. Here, we investigated the efficacy of PLCe knockdown to MNU induced bladder tumor and its possible mechanism. First, a plasmid contains small hairpin Ribonucleic acid (RNA) against PLC e was constructed. Then, this plasmid were intravesically installed into SD rats to silence the expression of PLC e. 40 PLC e silenced SD rats and 40 normal rats were intravesically installed with MNU, respectively. Another 10 normal SD rats were intravesically installed with saline. 12 weeks after installation, all rats were sacrificed. The bladders were harvested for pathological and histological examination, Reverse transcription polymerase chain reaction (RT-PCR) and Western-blotting. The pathological and histological examination results showed that 35 rats appeared tumor in normal rats group, while no rats appeared tumor in PLC e silenced group and saline group. RT-PCR and Western-blotting showed PLC e , PCNA were overexpressed in 35 tumor appeared rats and lowly expressed in other rats. The results reveal that the PLCe knockdown could interrupt the signal transduction in order to prevent MNU induced rats bladder tumorigenesis. Key words: PLCe, knockdown, MNU, Ras signal pathway and mechanism.
Highlights
Methyl-nitroso-urea (MNU) is a common carcinogen in laboratory
The results reveal that the PLCε knockdown could interrupt the signal transduction in order to prevent MNU induced rats bladder tumorigenesis
MNU were purchased from Applichem Corp (Germany); PLC ε, Cyclin-D1, proliferating cell nuclear antigen (PCNA) antibody was purchased from Takara Corp (Japan); PCR, western-blotting products were purchased from ShangHai-Huashun Biotechnology Corp (China); H-Ras anti-body, immunohistochemical kit were purchased from Beijing-Zhongshan Biotechnology Corp (China)
Summary
Methyl-nitroso-urea (MNU) is a common carcinogen in laboratory. It has been reported to induce mammary and bladder carcinogenesis (EI-sohemy et al, 1996, Hicks, l980). Chen et al 1431 initially identified in Caenorhabditis elegans as a Ras binding protein (Song et al, 2001) It contains conserved Ras-interacting domain, including a C-terminal RA domains which interact directly with Ras-family GTPases and an N-terminal CDC25 domain which impacts guanine nucleotide exchange activity to the protein (Kelly et al, 2001; Bunney and Katan, 2006). It has been reported closely related with the development of skin and colorectal tumor (Shuzo et al, 2008; Mingzhen et al, 2009). We determined the singal pathway by which PLC ε knockdown prevented MNU induced bladder tumorigenesis
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