首页> 中文期刊> 《海南医科大学学报(英文版)》 >Changes of PI3K/AKT/mTOR signaling pathway in the progression of cervical cancer and its target genes

Changes of PI3K/AKT/mTOR signaling pathway in the progression of cervical cancer and its target genes

         

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cqvip:Objective: To study the changes of PI3K/AKT/mTOR signaling pathway in the progression of cervical cancer and explore its target genes. Methods: The patients who underwent surgical resection and were diagnosed with cervical cancer by postoperative pathology in the First People's Hospital of Jiangxia District Wuhan City between June 2014 and December 2017 were selected, and the cervical cancer lesion tissues and lesion tissues adjacent to cervical cancer were kept;patients who underwent conization and were diagnosed with cervical intraepithelial neoplasia by postoperative pathology in the First People's Hospital of Jiangxia District Wuhan City during the same period were selected, and the cervical intraepithelial neoplasia tissues were kept. The protein levels of PI3K/AKT/mTOR signaling molecules as well as the mRNA expression of proliferation genes and invasion genes were determined. Results: p-PI3K, p-AKT, mTOR, p70S6K and p-4EBP1 protein levels as well as CyclinD1, Survivin, Piwil2, RACK1, EFEMP1 and VEGF mRNA expression in cervical cancer lesion tissues were significantly higher than those in adjacent lesion tissues and cervical intraepithelial neoplasia tissues whereas THBS2, Beclin1, E-cadherin, TIMP1 and TIMP2 mRNA expression were significantly lower than those in adjacent lesion tissues and cervical intraepithelial neoplasia tissues;p-PI3K, p-AKT, mTOR, p70S6K and p-4EBP1 protein levels in cervical cancer lesion tissues were positively correlated with CyclinD1, Survivin, Piwil2, RACK1, EFEMP1 and VEGF mRNA expression, and negatively correlated with THBS2, Beclin1, E-cadherin, TIMP1 and TIMP2 mRNA expression. Conclusion: Excessive activation of PI3K/AKT/mTOR signaling pathway during the progression of cervical cancer can change the expression of multiple proliferation and invasion genes to promote the proliferation and invasion of cancer cells.

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