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Expression of mTOR signaling pathway in adrenocortical tumour and its relationship with cell invasion and angiogenesis
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作者 sheng-ping tian Chong-Shan Wang Wei-Zhong Yang 《Journal of Hainan Medical University》 2018年第11期69-72,共4页
Objective:To study the expression of mTOR signaling pathway in adrenocortical tumour and its relationship with cell invasion and angiogenesis.Methods:Adrenocortical malignant tumor tissues and normal adrenal cortex ti... Objective:To study the expression of mTOR signaling pathway in adrenocortical tumour and its relationship with cell invasion and angiogenesis.Methods:Adrenocortical malignant tumor tissues and normal adrenal cortex tissues surgically removed in the Third People's Hospital of Huizhou Guangdong Province between September 2014 and February 2018 were selected, the protein was extracted to determine the expression of mTOR signaling molecules, and the RNA was extracted to determine the mRNA expression of cell invasion molecules and angiogenesis molecules.Results: p-PI3K, p-AKT, p-mTOR, p-S6K1 and p-4E-BP1 protein expression as well as MMP2, MMP9, PKC , VEGF and nm23-H1 mRNA expression in adrenocortical malignant tumor tissue were significantly higher than those in normal adrenal cortex tissue whereas PCAF, E-cadherin and TSP1 mRNA expression were significantly lower than those in normal adrenal cortex tissue;Pearson correlation analysis showed that p-PI3K, p-AKT, p-mTOR, p-S6K1 and p-4E-BP1 protein expression in adrenocortical malignant tumor tissue were negatively correlated with PCAF, E-cadherin and TSP1 mRNA expression, and positively correlated with MMP2, MMP9, PKC , VEGF and nm23-H1 mRNA expression.Conclusion:The excessive activation of mTOR signaling pathway in adrenocortical malignant tumor can promote cell invasion and angiogenesis. 展开更多
关键词 Adrenocortical MALIGNANT tumor MAMMALIAN target of RAPAMYCIN INVASION ANGIOGENESIS
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Relationship of GPRC6A and PKCzeta expression levels in prostate cancer lesions with cell proliferation and EMT
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作者 Fan-Fei Zeng sheng-ping tian +1 位作者 Wei-Zhong Yang Xiao-Yue Zhang 《Journal of Hainan Medical University》 2017年第15期145-148,共4页
Objective: To study the relationship of GPRC6A and PKCzeta expression levels in prostate cancer lesions with cell proliferation and epithelial-mesenchymal transition (EMT). Methods:Patients with prostate cancer and pa... Objective: To study the relationship of GPRC6A and PKCzeta expression levels in prostate cancer lesions with cell proliferation and epithelial-mesenchymal transition (EMT). Methods:Patients with prostate cancer and patients with benign prostatic hyperplasia who received surgical resection in Huizhou Third People's Hospital between June 2014 and March 2017 were selected, right amount of prostate cancer tissue and tissue adjacent to carcinoma was collected from patients with prostate cancer, and the expression of GPRC6A, PKCzeta, cell proliferation genes and EMT genes in lesions were detected. Results: GPRC6A, Survivin, SRSF1, Bcl-xl, N-cadherin and Vimentin expression in prostate cancer lesions and adjacent lesions were significantly higher than those in benign prostatic hyperplasia lesions while PKCzeta, Caspase-3, Caspase-9, Apaf-1, E-cadherin and CK5/6 expression were significantly lower than those in benign prostatic hyperplasia lesions;Survivin, SRSF1 and Bcl-xl expression in prostate cancer lesions with lower PKCzeta expression were significantly higher than those in prostate cancer lesions with higher PKCzeta expression while Caspase-3, Caspase-9 and Apaf-1 expression were significantly lower than those in prostate cancer lesions with higher PKCzeta expression;E-cadherin and CK5/6 expression in prostate cancer lesions with lower GPRC6A expression were significantly higher than those in prostate cancer lesions with higher GPRC6A expression while N-cadherin and Vimentin expression were significantly lower than those in prostate cancer lesions with higher GPRC6A expression. Conclusion:Highly expressed GPRC6A and lowly expressed PKCzeta in prostate cancer lesions can promote cell EMT and proliferation respectively. 展开更多
关键词 PROSTATE cancer G-protein-coupled receptor C6A Protein kinase Proliferation Epithelial-mesenchymal transition
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