Abstract

Gastric cancer (GC) is one of the most frequent cancers, resulting in plenty of death worldwide. Brassinin is a plant antibiotic extracted from cruciferous vegetables and exerts a vital anticancer role in various cancers. Nevertheless, its function and mechanism in GC are still uncovered. The role of brassinin in proliferation in GC cells were tested with cell counting kit 8 (CCK-8) or 5-ethynyl-2′-deoxyuridine (EdU) assay. The apoptotic cells were observed utilizing flow cytometry assay. Transwell analysis was introduced to assess GC cell migration as well as invasion. The downstream pathway regulated via brassinin in GC cells was determined utilizing Cignal Finder RTK signaling 10-Pathway Reporter Array and verified with Western blot assay. Brassinin reduced GC cell viability in a concentrated-dependent way. The brassinin treatment blocked cell migration in addition to invasion, and induced apoptosis in GC cells. Additionally, brassinin administration inactivated the NF-κB cascade signal. Meanwhile, NF-κB activator counteracted the effects of brassinin on GC cell progression. This investigation pointed out that brassinin inhibited growth and induced apoptosis at least partly by mediating NF-κB pathway in GC cells, which indicated that brassinin will be a promising drug for treating GC.

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