| 李儒彩,黄成谋,李静,等.磷脂酰肌醇 -4，5-二磷酸 3-激酶催化亚基 α通过调控跨膜受体蛋白 1对子宫内膜癌病人中性粒细胞的影响[J].安徽医药,2023,27(4):733-737. |
| 磷脂酰肌醇 -4，5-二磷酸 3-激酶催化亚基 α通过调控跨膜受体蛋白 1对子宫内膜癌病人中性粒细胞的影响 |
| Effect of PIK3CA on blood neutrophils in endometrial cancer patients by regulating Notch1 |
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| DOI：10.3969/j.issn.1009-6469.2023.04.022 |
| 中文关键词: 子宫内膜肿瘤 细胞增殖 磷脂酰肌醇 -4，5-二磷酸 3-激酶催化亚基 α(PIK3CA) 跨膜受体蛋白 1 中性粒细胞 |
| 英文关键词: Endometrial neoplasms Cell proliferation Phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) Transmembrane receptor protein 1 Neutrophil |
| 基金项目:海南省卫生健康行业科研项目( 20A200431) |
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| 中文摘要: |
| 目的探究磷脂酰肌醇 -4，5-二磷酸 3-激酶催化亚基 α(PIK3CA)基因通过调控跨膜受体蛋白 1(Notch1)的表达对子宫内膜癌病人血中性粒细胞的影响。方法选择 2020年 3月至 2021年 9月在海南医学院第一附属医院接受治疗的 50例子宫内膜癌病人(病例组)和 50例健康女性(对照组)为分析对象。检测病例组和实验组血清中中性粒细胞(NE)淋巴细胞(LY)、血红蛋白(Hb)血小板(PLT)计算 NLR指数(中性粒细胞计数 /淋巴细胞计数)。逆转录 PCR(RT-PCR)和Western、blotting检测 PIK3CA和 Notch1的、相对表达量，。选取人原髓细胞白血病细胞 /全反式维甲酸细胞( HL-60/ATRA细胞)，在不同时间下进行培养，验证 PIK3CA通过 Notch1对 NE的影响。结果病例组病人 NE、LY、PLT指标以及 NLR指数为(6.03±0.40)×109/L、(2.15±0.31)×109/L、(257.40±37.51)×109/L、(3.69±0.41)分别高于对照组的( 5.13±0.50)×109/L、(1.68±0.16)×109/L、(202.10±23.39)×109/L、(2.44±0.39)，病例组病人 Hb水平为( 138.72±13.79)g/L低于对照组 Hb水平( 149.52±10.65)g/L，说明子宫内膜癌病人炎症微环境异常。病例组 PIK3CA和 Notch1相对表达量为(3.351±0.496)、(3.467±0.440)高于对照组的(1.581±0.275)、(1.519±0.279)。HL-60/ATRA细胞培养实验验证了 PIK3CA高表达促进 Notch1高表达进而抑制 NE的增殖。结论在 NE中， Notch1表达量随着 PIK3CA表达量升高而升高， NE细胞活力逐渐下降，初步证实了 PIK3CA基因通过调控 Notch1的表达对子宫内膜癌中 NE产生影响。 |
| 英文摘要: |
| Objective To investigate the effect of the phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha(PIK3CA) gene on blood neutrophils in endometrial cancer patients by regulating the expression of transmembrane receptor protein 1(Notch1).Methods Fifty patients with endometrial cancer (case group) and 50 healthy women (control group) who received treatmentat the First Affiliated Hospital of Hainan Medical College from March 2020 to September 2021 were selected for analysis. Neutrophils(NE), lymphocytes (LY), hemoglobin (Hb) and platelets (PLT) were detected in the serum of the case group and the experimental group,and the NLR index (neutrophil count/lymphocyte count) was calculated. Reverse transcription PCR (RT-PCR) and Western blottingwere performed to detect the relative expression of PIK3CA and Notch1. Human promyelocytic leukemia cells/all-trans retinoid cells (HL-60/ATRA cells) were selected and cultured at different times to verify the effect of PIK3CA on NE via Notch1.Results NE, LY, PLT indexes and NLR index of patients in the case group were (6.03±0.40) ×109/L, (2.15±0.31) ×109/L, (257.40±37.51) ×109/L, and (3.69±0.41), respectively, which were higher than those of the control group (5.13±0.50)×109/L, ( (1.68±0.16)×109/L, (202.10±23.39)× 109/L, and (2.44±0.39), and the Hb level of patients in the case group was (138.72±13.79) g/L, which was lower than that of the controlgroup (149.52±10.65) g/L, indicating an abnormal inflammatory microenvironment in patients with endometrial cancer. The expressionlevels of PIK3CA and Notch1 in the case group were (3.351±0.496) and (3.467±0.440), respectively, which were higher than those inthe control group (1.581±0.275 and 1.519±0.279, respectively). HL-60/ATRA cell culture experiments verified that high expression ofPIK3CA promoted high expression of Notch1 and thus inhibited NE proliferation.Conclusion In NE, Notch1 expression increasedwith higher PIK3CA expression, and NE cell viability gradually decreased, tentatively confirming the effect of the PIK3CA gene on NEin endometrial cancer by regulating Notch1 expression. |
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