| 李 捷,刘紫蒙,郑一琼,解梦博,王正棠.乳腺浸润性导管癌组织IRS1、PRSS3蛋白表达与磷酸化蛋白激酶B表达和预后的关系研究[J].现代生物医学进展英文版,2021,(24):4617-4622. |
| 乳腺浸润性导管癌组织IRS1、PRSS3蛋白表达与磷酸化蛋白激酶B表达和预后的关系研究 |
| Relationship Research between the IRS1, PRSS3 Protein Expression and Phosphorylated Protein Kinase B Expression and Prognosis in Breast Invasive Ductal Carcinoma |
| Received:June 02, 2021 Revised:June 25, 2021 |
| DOI：10.13241/j.cnki.pmb.2021.24.003 |
| 中文关键词: 乳腺浸润性导管癌 胰岛素受体底物1 丝氨酸蛋白酶3 磷酸化蛋白激酶B 病理特征 预后 |
| 英文关键词: Breast invasive ductal carcinoma Insulin receptor substrate 1 Serine proteinase-3 Phosphorylated protein kinase B Pathological characteristics Prognosis |
| 基金项目:北京市科技计划项目（D171100006517004） |
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| 中文摘要: |
| 摘要 目的：探讨乳腺浸润性导管癌（BIDC）组织胰岛素受体底物1（IRS1）蛋白、丝氨酸蛋白酶3（PRSS3）蛋白表达与磷酸化蛋白激酶B（p-AKT）表达以及预后的关系。方法：选择2017年1月至2018年12月我院收治的363例BIDC患者，采用免疫组化法检测经手术切除的BIDC癌组织和癌旁组织中IRS1蛋白、PRSS3蛋白以及p-AKT表达，比较BIDC不同病理特征IRS1蛋白、PRSS3蛋白表达差异。Spearman秩相关分析IRS1蛋白、PRSS3蛋白表达与p-AKT表达的相关性。术后定期随访，采用Kaplan-Meier生存分析、Cox风险比例回归分析IRS1蛋白、PRSS3蛋白表达与BIDC患者预后的关系。结果：BIDC组织中IRS1蛋白、PRSS3蛋白、p-AKT阳性表达率分别为68.87%、58.13%、68.04%，均高于对照组的46.56%、40.50%、41.60%（P＜0.05）。IRS1蛋白表达、PRSS3蛋白表达与p-AKT表达均呈正相关（rs=0.805、0.796，P＜0.05）。肿瘤直径＞2 cm、低中度分化、AJCC分期为Ⅱ期的患者IRS1蛋白阳性表达率高于肿瘤直径≤2cm、高度分化、AJCC分期为Ⅰ期的患者（P＜0.05），AJCC分期为Ⅱ期、HER-2阳性表达、Ki-67阳性表达的患者PRSS3蛋白阳性表达率高于AJCC分期为Ⅰ期、HER-2阴性表达、Ki-67阴性表达的患者（P＜0.05）。Kaplan-Meier生存分析显示IRS1蛋白、PRSS3蛋白阳性表达者PFS生存率、OS生存率低于IRS1蛋白、PRSS3蛋白阴性表达者（P＜0.05）。多因素COX风险比例回归结果显示AJCC分期Ⅲ期、IRS1蛋白阳性表达、PRSS3蛋白阳性表达是BIDC患者预后不良的危险因素（P＜0.05）。结论：BIDC癌组织中IRS1蛋白、PRSS3蛋白阳性表达率增高，IRS1蛋白、PRSS3蛋白可能通过调节p-AKT参与BIDC癌症进展过程。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the relationship between the insulin receptor substrate 1 (IRS1) protein, serine proteinase 3 (PRSS3) protein expression and the phosphorylated protein kinase B (p-AKT) expression and prognosis in breast invasive ductal carcinoma (BIDC). Methods: 363 patients with BIDC who were admitted to our hospital from January 2017 to December 2018 were selected. Immunohistochemical method was used to detect the IRS1 protein, PRSS3 protein and p-AKT expression in surgically resected BIDC cancer tissues and paracancerous tissues. The expression differences of IRS1 protein and PRSS3 protein in different pathological characteristics of BIDC were compared. Spearman rank correlation analysis was used to analyze the correlation between the IRS1 protein, PRSS3 protein expression and p-AKT expression. Postoperative follow-up was performed regularly. Kaplan-Meier survival analysis and Cox risk ratio regression were used to analyze the relationship between the IRS1 protein and PRSS3 protein expression and the prognosis of patients with BIDC. Results: The positive expression rates of IRS1 protein, PRSS3 protein and p-AKT in BIDC tissue were 68.87%, 58.13% and 68.04%, respectively, which were all higher than 46.56%, 40.50% and 41.60% in control group(P<0.05). The IRS1 protein expression, PRSS3 protein expression were positively correlated with p-AKT expression (rs=0.805, 0.796, P<0.05). The positive expression rate of IRS1 protein in patients with tumor diameter > 2 cm, low to moderate differentiation and AJCC stage II were higher than that in patients with tumor diameter ≤2 cm, high differentiation and AJCC stage I (P<0.05). The positive expression rate of PRSS3 protein in patients with AJCC stage II, HER-2 positive expression and Ki-67 positive expression were higher than that in patients with AJCC stage I, HER-2 negative expression and Ki-67 negative expression(P<0.05). Kaplan-Meier survival analysis showed that the PFS survival rate and OS survival rate of patients with positive expression of IRS1 protein and PRSS3 protein were lower than those with negative expression of IRS1 protein and PRSS3 protein(P<0.05). Multivariate COX proportional regression analysis showed that AJCC stage Ⅲ, IRS1 protein positive expression and PRSS3 protein positive expression were risk factors for poor prognosis of patients with BIDC(P<0.05). Conclusion: The positive expression rates of IRS1 protein and PRSS3 protein in BIDC cancer tissues are increased, and IRS1 protein and PRSS3 protein may participate in the progression of BIDC cancer by regulating p-AKT. |
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