新辅助化疗不同给药方式治疗晚期宫颈癌的疗效及其机制

Clinical Efficacy and Mechanism of Different Neoadjuvant Chemotherapy Administrations in the Treatment of Advanced Cervical Cancer

【目的】探讨新辅助化疗(紫杉醇+顺钳)不同给药方式治疗晩期宫颈癌的临床疗效及其机制。【方法】选取2016年3月至2018年3月在本院接受新辅助化疗的晚期宫颈癌患者68例.按照随机数表法分为介入组(新辅助介入动脉化疗)和静脉组(新辅助静脉化疗).每组34例。比较两组患者近期的疗效及不良反应,检测两组患者癌组织中PI3K/AKT/mTOR信号通路的相关因子磷酸化胞内磷脂酰肌醇激酶(p-PI3K)、磷酸化蛋白激酶B(p-Akt)、磷酸化雷帕霉素靶蛋白(p-mTOR).基质金属蛋白酶2(MMP2)、血管内皮生长因子(VEGF)水平并分析其作用机制。【结果】介入组患者有效率显著高于静脉组,不良反应发生率显著低于静脉组(P<0.05);介入组患者宫颈癌组织中的p-PI3K、p-Akt、p-mTOR、MMP2、VEGF蛋白水平均显著低于静脉组(P<0.05).【结论】新辅助介入动脉化疗治疗晚期宫颈癌的近期疗效明显优于新辅助静脉化疗,且能有效地抑制宫颈癌组织细胞中的PI3K/AKT/mTOR信号通路,这可能与显著抑制其磷酸化有关。

[Objective]To investigate the expression of PI3K/AKT/mTOR signaling pathway and clinical efficacy of different Neoadjuvant Chemotherapy administration (Paclitaxel + Cisplatin) for advanced cervical cancer.[Methods]From March 2016 to March 2018, 68 patients with advanced cervical cancer who received neoadjuvant chemotherapy in Boai Hospital of Zhongshan City were selected. According to the random table method, they were divided into the interventional group ( neoadjuvant interventional arterial chemotherapy) and the intravenous group (neoadjuvant intravenous chemotherapy), with 34 cases in each group. The levels of p-PI3K, p-Akt, p-mTOR, matrix metalloprotease 2 (MMP2) and vascular endothelial growth factor (VEGF) were compared between the two groups. The short-term efficacy and adverse reactions were recorded and compared as well.[Resulis]The effective rate of the intervention group was higher than that of the intravenous group, and the incidence of adverse reactions was lower than that of the intravenous group ( P <0.05). The levels of p-PI3K, p-Akt, p-mTOR, MMP2 and VEGF protein in cervical cancer tissues of intervention group were significantly lower than those of venous group ( P <0.05).[Conclusion]The short-term efficacy of neoadjuvant interventional arterial chemotherapy for advanced cervical cancer treatment is better than neoadjuvant intravenous chemotherapy. It can effectively inhibit the PI3K/AKT/mTOR signaling pathway in cervical cancer cells, which may be related to the significant inhibition of its phosphorylation.