Abstract
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.
Obovatol inhibits the growth and aggressiveness of tongue squamous cell carcinoma through regulation of the EGF‑mediated JAK‑STAT signaling pathway
