Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Table 1 The antitumor activity of sanguinarine

Sanguinarine induces apoptosis in tumor cells through multiple pathways, including the activation of NF-κB, the mitochondrial damage and cell cycle arrest

Sanguinarine-induced apoptosis is associated with the decrease of Bcl-2 and the increase of Bax proteins and the generation of reactive oxygen species

Sanguinarine causes cell cycle arrest by increasing the expression of p27 and decreasing cyclin D1, D2 and E, and CDK2, 4 and 6

Sanguinarine inhibits tumor progression associated with chronic inflammation via the inhibition of NF-κB

Sanguinarine inhibits tumor angiogenesis through the inhibition of VEGF secretion and VEGF signal transduction (Akt, p38 and VE-cadherin)

Sanguinarine has an inhibitory effect on tumor cell migration by the inhibition of MMP-9 and STAT3 activation

Sanguinarine exerts a synergistic effect with chemotherapeutic agents and enhances the chemosensitivity of Caco 2 and CEM/ADR5000 adryamicin-resistant leukemia cells

NF-κB: Nuclear factor-κB; CDK: Cyclin-dependent kinase; Bcl: B cell lymphoma; VEGF: Vascular endothelial growth factor; STAT: Signal transducer and activator of transcription.