Epithelial transformation sequence 2 affecting the in vitro metastatic activity of esophageal squamous carcinoma cells by regulating the expression of p33 inhibitor growth-1
10.16098/j.issn.0529-1356.2024.02.011
- VernacularTitle:上皮细胞转化序列2通过调控p33生长抑制因子1表达影响食管鳞状细胞癌细胞的体外转移活性
- Author:
Yang WANG
1
;
Zhen-Hua WU
;
Hong-Bo LÜ
;
Dong-Bo LUO
Author Information
1. 新疆医科大学附属肿瘤医院胸外科二病区,乌鲁木齐 830011
- Keywords:
Epithelial cell transformation sequence 2;
p33 inhibitor of growth-1;
Esophageal squamous carcinoma;
Metastasis;
Western blotting
- From:
Acta Anatomica Sinica
2024;55(2):203-209
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of epithelial transformation sequence 2(ECT2)and p33ING1 on the metastatic activity of esophageal squamous cell carcinoma(ESCC)cells.Methods The expressions of ECT2 and p33ING1 in esophageal squamous cell carcinoma tissues and adjacent tissues were detected by immunohistochemistry and Western blotting.Human esophageal squamous carcinoma cell line KYSE140 cells were divided into 4 groups:blank group,negative control(pcDNA 3.1 NC)group,overexpression group(pcDNA 3.1 ECT2)and inhibited expression group(si ECT2).MTT assay and cell colony formation assay were used to study the proliferation and growth ability of cells,Transwell assay and scratch assay used to study the invasion and migration ability of cells,and flow cytometry used to detect apoptosis and cell cycle,Western blotting used to detect the effect of ECT2 on p33ING1 protein.Results ECT2 expression increased and p33ING1 expression decreased in esophageal squamous cell carcinoma tissues.Overexpression of ECT2 significantly increased the growth,colony formation,migration and invasion abilities of KYSE140 cells,and decreased the apoptosis rate and p33ING1 expression of KYSE140 cells.In addition,inhibition of ECT2 expression could reverse the above changes.Conclusion The high expression of ECT2 can promote the growth and metastasis of esophageal squamous cell carcinoma KYSE140 cells and inhibit their apoptosis.The mechanism may be related to the inhibition of p33ING1 expression by ECT2.
