Department of Pathophysiology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi, China.
The second Department of Gastroenterology, the First Affiliated Hospital, Xinjiang Medical University, Urumqi, China.
J Physiol Pharmacol. 2023 Oct;74(5). doi: 10.26402/jpp.2023.5.07. Epub 2023 Dec 6.
This study aimed to observe the differential expression of Annexin-A1 in esophageal squamous cell carcinoma (ESCC) and explored the effect of small interfering ribonucleic acid (RNAi)-Annexin-A1 on the biological behavior of CE81T-0 cells. An immunohistochemical approach was used to detect the expression of Annexin-A1 in 86 pairs of ESCC samples. Quantitative reverse transcription polymerase chain reaction was used to detect the expression of Annexin-A1 in CE81T-0 and CE81T-4 cells, and the expression of Annexin-A1 in CE81T-0 cells was knocked out by RNAi. A methyl-thiazolyl-tetrazolium assay was used to observe the effect of Annexin-A1 on cell proliferation, and flow cytometry was conducted to analyze its effect on cell cycles and apoptosis. A scratch assay and a Transwell chamber were used to detect changes in cell migration and invasion. From the results, compared with the Annexin-A1 expression rate of 59.3% in para-carcinoma tissues, the expression of Annexin-A1 in cancer was reduced to only 32.6% in ESCC cells. Annexin-A1 was strongly expressed in highly differentiated ESCC cells without lymphatic metastasis and highly expressed in the CE81T-0 cell group with low metastasis. Annexin-A1 gene silencing promoted cell proliferation and inhibited apoptosis, blocked cells in the S-phase, and increased cell migration, leading to an increase in the number of invaded cells. Above all, Annexin-A1 could reflect the differentiation degree and lymph node metastasis of ESCC cells to some extent and was involved in the invasion, metastasis, proliferation, and other biological behaviors of ESCC cells, indicating an experimental basis for Annexin-A1 as a molecular marker in the early diagnosis of ESCC and the prediction of cell metastasis, invasion, and differentiation degree.
本研究旨在观察膜联蛋白 A1 在食管鳞状细胞癌(ESCC)中的差异表达,并探讨小干扰核糖核酸(RNAi)-膜联蛋白 A1 对 CE81T-0 细胞生物学行为的影响。采用免疫组织化学方法检测 86 对 ESCC 标本中膜联蛋白 A1 的表达。采用定量逆转录聚合酶链反应检测 CE81T-0 和 CE81T-4 细胞中膜联蛋白 A1 的表达,并通过 RNAi 敲除 CE81T-0 细胞中的膜联蛋白 A1。噻唑蓝比色法观察膜联蛋白 A1 对细胞增殖的影响,流式细胞术分析其对细胞周期和凋亡的影响。划痕试验和 Transwell 室检测细胞迁移和侵袭的变化。结果显示,与癌旁组织中膜联蛋白 A1 表达率为 59.3%相比,ESCC 细胞中膜联蛋白 A1 的表达降低至仅 32.6%。膜联蛋白 A1 在无淋巴转移的高分化 ESCC 细胞中强烈表达,在低转移的 CE81T-0 细胞组中高表达。膜联蛋白 A1 基因沉默促进细胞增殖,抑制细胞凋亡,使细胞阻滞在 S 期,并增加细胞迁移,导致侵袭细胞数量增加。综上所述,膜联蛋白 A1 可以在一定程度上反映 ESCC 细胞的分化程度和淋巴结转移,参与 ESCC 细胞的侵袭、转移、增殖等生物学行为,为膜联蛋白 A1 作为 ESCC 早期诊断和预测细胞转移、侵袭和分化程度的分子标志物提供了实验依据。