A clinical study on the expression of PTEN in renal cell carcinoma in children
Hong Lu, Yuxia Tan, Liping Chen
Abstract
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Hong Lu, Yuxia Tan, Liping Chen
Abstract
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The expression pattern of tumor suppressor gene phosphatase and tensin homolog deleted on chromosome ten (PTEN) and phosphatase and tensin homolog deleted on chromosome ten/phosphatidylinositol3-kinase/protein kinase B (PTEN/PI3K/AKT) cell signaling pathway in renal cell carcinoma (RCC) were investigated in children. A total of 5 cases of RCC (observation group) in children and 10 cases of benign kidney tumor (control group) diagnosed by pathological examinations were included to obtain tumor samples. Expression of PTEN mRNA was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The protein expression of PTEN, PI3K and AKT was detected by western blotting; relationships between the expression level of PTEN mRNA and the clinical features of RCC were analyzed. It turned out that expression level of PTEN mRNA in the observation group was significantly lower than that in the control group. The protein expression levels of PTEN, PI3K and AKT were significantly lower in the observation group than in the control group (P<0.05). The expression level of PTEN mRNA decreased with the increased clinical stage of RCC (P<0.05), and was not related to sex, age and maximum tumor diameter (P>0.05). The results showed that downregulation of the tumor suppressor gene PTEN expression and the inhibition of PTEN/PI3K/AKT cell signaling pathway may be involved in the occurrence and development of RCC in children.
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The expression pattern of tumor suppressor gene phosphatase and tensin homolog deleted on chromosome ten (PTEN) and phosphatase and tensin homolog deleted on chromosome ten/phosphatidylinositol3-kinase/protein kinase B (PTEN/PI3K/AKT) cell signaling pathway in renal cell carcinoma (RCC) were investigated in children. A total of 5 cases of RCC (observation group) in children and 10 cases of benign kidney tumor (control group) diagnosed by pathological examinations were included to obtain tumor samples. Expression of PTEN mRNA was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The protein expression of PTEN, PI3K and AKT was detected by western blotting; relationships between the expression level of PTEN mRNA and the clinical features of RCC were analyzed. It turned out that expression level of PTEN mRNA in the observation group was significantly lower than that in the control group. The protein expression levels of PTEN, PI3K and AKT were significantly lower in the observation group than in the control group (P<0.05). The expression level of PTEN mRNA decreased with the increased clinical stage of RCC (P<0.05), and was not related to sex, age and maximum tumor diameter (P>0.05). The results showed that downregulation of the tumor suppressor gene PTEN expression and the inhibition of PTEN/PI3K/AKT cell signaling pathway may be involved in the occurrence and development of RCC in children.
Key concepts: PTEN, Oncogene, Molecular medicine, Renal cell carcinoma, Cell cycle, Cancer research, Cancer, Cell