Karanjin is a bioactive furanoflavonoid with various pharmacological activities including anticancer activities. However, the effect and the related mechanism of
karanjin in
breast cancer (BC) have not been revealed. The potential targets of
karanjin and BC were predicted using SwissTargetPrediction and GeneCards databases, respectively. The overlapping targets between
karanjin and BC were identified using the Venn diagram. DAVID database was used for the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment pathway analysis. Cell viability, proliferation, and apoptosis were examined by MTT (3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-tetrazolium bromide), EdU (5-ethynyl-2'-deoxyuridine) incorporation, and TUNEL (
terminal deoxynucleotidyl transferase-mediated dUTP
digoxigenin nick-end labeling) assays, respectively. The
protein levels were measured by western blot analysis. We screened out 28 overlapping targets between
karanjin and BC. KEGG analysis showed that the targets of
karanjin in BC were associated with the
phosphatidylinositol 3-kinase (PI3K)/
protein kinase B (Akt) pathway.
Karanjin inhibited cell viability and impeded the proliferative ability of BC cells. Moreover,
karanjin treatment induced apoptosis in BC cells. Additionally,
karanjin treatment blocked the PI3K/Akt signaling pathway and activation of the PI3K/Akt pathway reversed the antitumor effect of
karanjin on BC cells. In conclusion,
karanjin exerted antitumor activity in BC cells by regulating the PI3K/Akt signaling pathway.