首页|长链非编码RNA467调控SATB1活性促进子宫内膜癌增殖、侵袭机制研究

长链非编码RNA467调控SATB1活性促进子宫内膜癌增殖、侵袭机制研究

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目的:探讨长链非编码RNA467是否通过调控SATB1进而激活PI3K/Akt通路影响子宫内膜癌的进展.方法:通过搜索(http://starbase.sysu.edu.cn)找到与LINC00467相结合的靶mRNA(SATB1),培养正常子宫内膜细胞和HEC-1A、Ishikawa细胞,通过转染序列实验及RT-qPCR、Western blot等方法逐步验证LINC00467通过调控SATB1影响PI3K/Akt通路进而促进子宫内膜癌细胞增殖、迁移和侵袭.结果:敲低LINC00467表达后,SATB1表达下降,差异有统计学意义(P<0.01).抑制SATB1后,p-Akt和p-PI3K表达下降,差异有统计学意义(P<0.01).转染pcDNA3.1-SATB1后,p-Akt和p-PI3K表达上升,差异有统计学意义(P<0.01).与空载组相比,sh-LINC00467#1组和sh-LINC00467#1+pcDNA3.1组p-Akt和p-PI3K表达量明显下降,EdU阳性细胞数明显减少,细胞克隆数明显减少,Bcl-2蛋白表达量明显下降,cleaved caspase 3蛋白表达量明显上升,细胞凋亡率明显增加,细胞迁移率明显下降,侵袭细胞数明显减少,差异均有统计学意义(P<0.01),而 sh-LINC00467#1+pcDNA3.1-SATB1 组 p-Akt 和 p-PI3K 表达量、EdU 阳性细胞数、细胞克隆数、Bcl-2和cleaved caspase 3蛋白表达量、细胞凋亡率、细胞迁移率、侵袭细胞数均无明显降低,差异均无统计学意义(P>0.05).结论:LINC00467通过促进SATB1进而激活PI3K/Akt通路促进子宫内膜癌细胞增殖、迁移和侵袭,抑制其凋亡.
Effect and mechanism of long-chain non-coding RNA467 on the proliferation and inva-sion of endometrial carcinoma by regulating SATB1 activity
Objective:To investigate whether long-chain noncoding RNA467 affects the progression of endometrial cancer by regulating SATB1 and activating PI3K/Akt pathway.Methods:Firstly,through the search(http://starbase.sysu.edu.cn)found target mRNA(SATB1)of LINC00467,normal endometrial cells,HEC-1A and Ishikawa cell were cultured.Transfection sequence experiments,RT-qPCR,Western blot and other methods were used to confirm that LINC00467 affected PI3K/Akt through the regulation of SATB1,thus promoting the proliferation,migration and invasion of endometrial cancer cells.Results:After knockdown the expression of LINC00467,the expression of SATB1 decreased,and the difference was statistical-ly significant(P<0.01).After SATB1 inhibition,the expressions of p-Akt and P-PI3K de-creased,and the differences were statistically significant(P<0.01).After transfection with pcDNA3.1-SATB1,the expressions of p-Akt and P-PI3K were increased,and the differences were statistically significant(P<0.01).Compared with the sh-NC group,the expression levels of p-Akt and p-PI3K in sh-LINC00467#1 and sh-LINC00467#1+pcDNA3.1 groups were sig-nificantly decreased,the number of EdU positive cells was significantly decreased,the number of cell clones was significantly decreased,and the expression level of Bcl-2 protein was signifi-cantly decreased,cleaved caspase 3 protein expression was significantly increased,apoptosis rate was significantly increased,cell mobility was significantly decreased,and the number of invasive cells was significantly decreased,with statistical significance(P<0.01).In the sh-LINC00467#l+pcDNA3.1-SATB1 group,the expression levels of p-Akt and p-PI3K,the number of EdU positive cells,the number of cell clones,the protein expression levels of Bcl-2 and cleaved caspase 3,the apoptosis rate,cell mobility,and the number of invasive cells were not significant-ly decreased.There were no significant differences(P>0.05).Conclusion:LINC00467 can promote the proliferation,migration and invasion of endometrial cancer cells and inhibit their apoptosis by promoting the expression of SATB1 and then activating PI3K/Akt pathway.

Endometrial cancerLong-chain noncoding RNA467SATB1Real-time fluorescence quantitative polymerase chain reactionFlow cytometry

王圆圆、关新垒、苗梦薇、杜昕、秦海霞

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新乡医学院第一附属医院妇科,卫辉 453100

子宫内膜癌 长链非编码RNA467 SATB1 实时荧光定量聚合酶链反应 流式细胞术

2025

现代妇产科进展
山东大学

现代妇产科进展

影响因子:1.089
ISSN:1004-7379
年,卷(期):2025.34(1)