The Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China; Provincial Cooperative Innovation Center for Cancer Chemoprevention, Zhengzhou University, Zhengzhou 450001, China; Cancer Chemoprevention International Collaboration Laboratory, Zhengzhou 450001, China.
The Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China; Provincial Cooperative Innovation Center for Cancer Chemoprevention, Zhengzhou University, Zhengzhou 450001, China; Second People's Hospital of Henan Province, Zhengzhou 451191, China.
Pathol Res Pract. 2022 Sep;237:154025. doi: 10.1016/j.prp.2022.154025. Epub 2022 Jul 14.
BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor of the digestive tract, which is very harmful to human health. The JAK-STAT signaling pathway is a recognized carcinogenic pathway that plays a role in the proliferation, apoptosis, migration, and invasion of a variety of cancer cells. Some studies have shown that the activation status of STAT3 affects the expression of KIRREL3. However, the expression of KIRREL3 in ESCC and its relationship with KIRREL3 or the JAK-STAT signaling pathway is still unclear. METHODS: In this study, we used immunohistochemistry and western blotting to analyze the protein expression levels of KIRREL3 in tumor tissues and ESCC cell lines. We applied proliferation assays, plate clone formation assays, Transwell assays, flow cytometry analysis, and CDX animal models to examine the role of KIRREL3 in ESCC. RESULTS: The results indicate that KIRREL3 is highly expressed to varying degrees in ESCC tissues and cell lines. Knocking down KIRREL3 expression in ESCC cells could correspondingly inhibit cell proliferation, colony formation, invasion, and migration, and had some effects on cell cycle progression and apoptosis. In addition, overexpressing KIRREL3 in these cells had opposite effects. Tumor formation in nude mice experiments also confirmed that KIRREL3 is involved in the growth of ESCC cells in vivo. CONCLUSIONS: These data suggest that KIRREL3 plays a key role in the development of ESCC, and KIRREL3 is a potential new target for the early diagnosis and clinical treatment of this disease.
背景：食管鳞状细胞癌（ESCC）是一种常见的消化道恶性肿瘤，对人类健康危害极大。JAK-STAT 信号通路是公认的致癌途径，在多种癌细胞的增殖、凋亡、迁移和侵袭中发挥作用。一些研究表明，STAT3 的激活状态影响 KIRREL3 的表达。然而，KIRREL3 在 ESCC 中的表达及其与 KIRREL3 或 JAK-STAT 信号通路的关系尚不清楚。
方法：本研究采用免疫组织化学和 Western blot 分析了肿瘤组织和 ESCC 细胞系中 KIRREL3 的蛋白表达水平。我们应用增殖实验、平板克隆形成实验、Transwell 实验、流式细胞术分析和 CDX 动物模型来研究 KIRREL3 在 ESCC 中的作用。
结果：结果表明，KIRREL3 在 ESCC 组织和细胞系中不同程度地高度表达。在 ESCC 细胞中敲低 KIRREL3 表达可相应抑制细胞增殖、集落形成、侵袭和迁移，并对细胞周期进程和细胞凋亡有一定影响。此外，过表达这些细胞中的 KIRREL3 则有相反的效果。裸鼠实验中的肿瘤形成也证实了 KIRREL3 参与了 ESCC 细胞在体内的生长。
结论：这些数据表明 KIRREL3 在 ESCC 的发展中起着关键作用，KIRREL3 是该疾病早期诊断和临床治疗的潜在新靶点。
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