Network pharmacology, as a novel way using bioinformatics to explore drug targets and interactions in
cancer, broadens our understanding of drug action, thereby facilitating drug discovery. Here, we utilized network pharmacology to explore the role and mechanism by which
cinobufotalin functions in
colon adenocarcinoma (
COAD). We found that
cinobufotalin represses the growth and proliferation of
colon cancer cells, and integrated public databases for targets reported to be associated with
COAD, together with those predicted to be targets of
cinobufotalin. Targets overlapped between
COAD-associated
proteins and
cinobufotalin target
proteins were used to filter candidate targets of
cinobufotalin in
COAD. The following
proteins were thought to occupy a key position in
COAD-
cinobufotalin target networks: SRC, PIK3R1, MAPK1, PIK3CA, HSP90AA1, CTNNB1, GRB2, RHO1, PTPN11, and EGFR. The networks regulated by
cinobufotalin were involved mainly in extracellular signal stimulation and transduction, including MAPK signaling pathway, PI3K-AKT signaling pathway, and JAK-STAT signaling pathway. Besides, transcriptome sequencing results also indicated that
cinobufotalin inhibits the response of
colon cancer cells to extracellular stimulation and promotes cell apoptosis. Molecular docking results showed that
cinobufotalin matches in the pocket of the top candidate
cinobufotalin target
proteins (SRC, PIK3R1, MAPK1 and PIK3CA). These findings demonstrate
cinobufotalin can be developed as potential anti-
cancer therapeutics.