UNBS5162 inhibits the proliferation of esophageal cancer squamous cells via the PI3K/AKT signaling pathway

C-X-C motif chemokine ligand (CXCL) signaling has been demonstrated to be involved in cancer invasion and migration; therefore, CXCL antagonists may serve as anticancer drugs by preventing tumor proliferation. The present study aimed to investigate whether a pan antagonist of CXCLs, UNBS5162, may inhibit esophageal cancer proliferation and to identify the underlying mechanisms. Cell proliferation and cell colony formation results, which were determined by a Cell Counting Kit-8 assay and crystal violet staining, respectively, demonstrated that UNBS5162 inhibited esophageal cancer cell proliferation. Following treatment with UNBS5162, Transwell migration and Matrigel invasion assays, and flow cytometry with Annexin V-fluorescein isothiocyanate and propidium iodide staining, were performed to investigate cell migration, invasion and apoptosis in human esophageal cancer cells. The results indicated that invasion and migration was reduced in UNBS5162-treated cells, while apoptosis was increased. Western blotting experiments confirmed that UNBS5162 downregulated the protein expression of proteins associated with the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway, including the levels of phosphorylated (p)-AKT, p-mechanistic target of rapamycin kinase, ribosomal protein S6 kinase 1 and cyclin D1. In addition, upregulated expression of programed cell death 4 was observed following UNBS5162 treatment. The present study demonstrated that UNBS5162 is a novel naphthalimide that may have potential therapeutic use for the prevention of esophageal cancer proliferation and metastasis via the PI3K/AKT signaling pathway.