|Table of Contents|

Cx32 regulates the malignant biological behavior of endometrial carcinoma cells through the PI3K/AKT pathway

Journal Of Modern Oncology[ISSN:1672-4992/CN:61-1415/R]

Issue:
2023 16
Page:
2995-3001
Research Field:
Publishing date:

Info

Title:
Cx32 regulates the malignant biological behavior of endometrial carcinoma cells through the PI3K/AKT pathway
Author(s):
GAO ShanTIAN PengpengHAN YanshuXIE ChiFENG ZixuanLI Yan
Department of Obstetrics and Gynecology,Central Hospital Affiliated to Shenyang Medical College,Liaoning Shenyang 110024,China.
Keywords:
endometrial carcinomaconnexin 32phosphorylated protein kinase BPI3K/AKT signaling pathwayepigenetic regulation
PACS:
R737.33
DOI:
10.3969/j.issn.1672-4992.2023.16.009
Abstract:
Objective:To observe the expression of connexin 32 (Cx32) and phosphorylated protein kinase B (p-AKT) in endometrial carcinoma tissues and cell lines,in order to explore the mechanism of Cx32 regulating the occurrence and development of endometrial carcinoma (EC) through phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) signaling pathway.Methods:The expression levels of Cx32 and p-AKT in EC tissues and normal endometrial tissues,normal endometrial epithelial cell line (hEEC) and two EC cell lines,Ishikawa (well differentiated) and KLE (poorly differentiated),were detected by immunohistochemistry and Western blotting (WB).Analyze the relationship between the two.By WB,Transwell,CCK-8 and scratch healing,the expression changes of Cx32 and p-AKT in each group before and after Cx32 overexpression and their effects on cell proliferation,invasion and migration were measured.Cx32-overexpressed Ishikawa and KLE cells were treated with PI3K/AKT signaling pathway inhibitors,and the proliferative activity of EC cells before and after transfection was detected by CCK-8 method.Results:The positive expression rate of Cx32 in EC tissues (62.50%) was significantly lower than that in normal endometrial tissues (100.00%).The positive expression rate of p-AKT in EC tissues (85.00%) was significantly higher than that in normal endometrial tissues (35.00%) (P<0.05).Cx32 expression was negatively correlated with the expression of p-AKT in EC tissues,with statistical significance (r=-0.325,P<0.05).Compared with hEEC cells,the expression level of Cx32 in Ishikawa and KLE cells decreased and the expression level of p-AKT increased,while the expression level of Cx32 in KLE cells was the lowest and the expression level of p-AKT was the highest.The cell proliferation,invasion and migration levels of Ishikawa cells were significantly lower than those of KLE cells (P<0.05).After overexpression of Cx32,the expression level of Cx32 was increased,the expression level of p-AKT was decreased,and the level of cell invasion and migration was significantly decreased (P<0.05).Cx32-overexpressed Ishikawa and KLE cells treated with PI3K/AKT signaling pathway inhibitors had lower cell viability than untreated Cx32-overexpressed Ishikawa and KLE cells (P<0.05).Conclusion:Cx32 can play a role in regulating the occurrence and development of EC through PI3K/AKT signaling pathway.Compared with normal endometrial tissues,Cx32 expression decreased and p-AKT expression increased in EC tissues.The expression of Cx32 in both cancer cells was lower than that in normal endometrial epithelial cells,and higher in Ishikawa cells than that in KLE cells (P<0.05).In order to further examine the regulatory role of Cx32 and PI3K/AKT signaling pathways in the progression of EC,Cx32 was overexpressed in Ishikawa and KLE cells,and the expression level of p-AKT was measured by WB.The results showed that when Cx32 was overexpressed in Ishikawa and KLE cells,the protein expression level of p-AKT was decreased,indicating the decreased activity of PI3K/AKT signaling pathway.The addition of PI3K/AKT signaling pathway inhibitors further verified that Cx32 may play a role in the occurrence and development of EC through PI3K/AKT signaling pathway.

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沈阳医学院硕士研究生科技创新基金项目(编号:Y20210520)
Last Update: 1900-01-01