Abstract
Similar effects are seen in colorectal carcinomas. It decreases Bcl-2 levels. At the same, time it augments Bax levels (Lee et al., 2012). These growth inhibitory effects are dose dependent. Caspase-3 activity is also markedly increased (Pica et al., 2012). Overall, this results in accentuated intratumoral apoptosis. PeritumoraL angiogenesis is also decreased. Similarly, sanguinarine decreases tumor growth in pulmonary malignancies. It mediates this effect by up regulating MKP-1 expression (Jang et al., 2009). It also causes attenuation of intracellular glutathione levels. As a result, it augments activation of caspase-3 and caspase- 9. All of these effects ultimately result in marked accentuation of intratumoral apoptosis.
Sanguinarine inhibits MMP-2 and MMP-9 activity in breast carcinomas (Choi et al., 2009). It also activates caspase-3 and caspase-9 activity secondary to augmented release of cytochrome c. It also augments transepithelial electrical resistance, thereby enhancing tight junction tightness. X-linked inhibitor of apoptosis protein (XIAP) levels are also attenuated (Choi et al., 2008). It also has an attenuating effect on claudin levels. Thus, apoptosis is enhanced while proliferation is decreased. This results in decreased invasiveness as well as metastasis. These antineoplastic effects are mediated in a dose dependent manner. Similar effects are seen in cervical carcinomas. It mediates its antineoplastic effect by up regulating Bax. At the same time, it down regulates Bcl-2 (Xu et al., 2012). As a result, it markedly accentuates intratumoral apoptosis. It also decreases NF-κB expression, thereby further augmenting tumoral apoptosis.
The above examples clearly exemplify the potent pro-apoptotic and antiproliferative effects of sanguinarine. Further studies are needed to fully evaluate its antineoplastic effects.
Footnotes
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No competing financial interests exist.