目的 探讨上皮细胞转化序列2（ECT2）与p33生长抑制因子1（p33ING1）的表达水平对食管鳞状细胞癌（ESCC）细胞转移活性的影响。  方法 采用免疫组织化学法和免疫印迹法检测食管鳞癌组织和癌旁组织中ECT2和p33ING1的表达情况。将人食管鳞癌细胞系KYSE140细胞分为4组：空白组、阴性对照组（pcDNA 3.1 NC）组、过表达组（pcDNA 3.1 ECT2）和抑制表达组（si ECT2）。采用MTT法和细胞集落形成实验研究细胞的增殖和生长能力，Transwell实验和划痕实验研究细胞的侵袭和迁移能力，并用流式细胞术检测细胞凋亡率和细胞周期，Western blotting检测ECT2对p33ING1蛋白的影响。  结果 在食管鳞癌组织中ECT2表达增加，p33ING1表达降低。过表达ECT2能够显著增加KYSE140细胞的生长、集落形成、迁移以及侵袭能力，并能降低KYSE140细胞的凋亡率和p33ING1的表达；此外，抑制ECT2表达后能够逆转上述变化。  结论 ECT2 高表达能够促进食管鳞癌 KYSE140 细胞的生长、转移，并抑制其凋亡，其机制可能与 ECT2 能够抑制 p33ING1 表达相关。

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.