Abstract:In this study, non-small cell lung cancer A549 was used as a model to determine the mechanism by which C-phycocyanin (C-PC) regulated the biological behavior of A549 cells. MTT assay, clonal formation assay, flow cytometry and scratch assay were used to examine the effects of C-PC on cell proliferation and migration. The key gene receptor interacting protein kinase 1 (RIPK1) was screened by transcriptome sequencing analysis, the silencing efficiency was detected by real-time PCR and western blot, and the effect of cell proliferation and migration capacity in vitro was verified by transfecting RIPK1 small interfering RNA. The C-PC reduced cell survival rate, growth rate, and cell colony formation ability. After transfecting RIPK1 siRNA, the expression level of RIPK1 was inhibited. Meanwhile, cell growth rate, colony formation and migration ability were suppressed. The cell cycle exerted G1 phase arrest. This work indicated that C-PC could inhibit the proliferation and migration of A549 cells by down-regulating RIPK1 expression level, which laid a foundation for the deep utilization of new anti-cancer functional food colorants. It also provides the necessary theory for the safe treatment of non-small cell lung cancer.