Abstract
Maslinic acid (2α, 3β-dihydroxyolean-12-en-28-oic acid, MA) was isolated from natural plants and showed anti-cancer activity in rat Pheochromocytoma PC12 cells in our previous studies. We now discover that MA disrupts the interaction between Bcl2 and autophagy scaffold protein Beclin1 in the above cell line, leading to the up-regulation of autophagy. We investigated the effect of MA on the interaction between Bcl2 and Beclin1 by biochemical and biophysical methods in combination with autophagy characterization in the above cell line. Our results suggest that MA may serve as an autophagy activator by directly blocking the Bcl2-Beclin1 interaction to release free Beclin1 required for the recruitment of autophagy positive regulators, implying MA may exert its anti-cancer activity by regulating autophagy.
Highlights
Maslinic acid, abbreviated from 2α, 3β-dihydroxyolean-12-en-28-oic acid, maslinic acid (MA), a member of triterpenes (Figure 1), is widely found in nature and is mainly present in olive-pomace oil, being the principal component of the wax-like coating in the olive skin [1]
Our results suggest that MA may serve as an autophagy activator by directly blocking the Bcl2-Beclin1 interaction to release free Beclin1 required for the recruitment of autophagy positive regulators, implying MA may exert its anti-cancer activity by regulating autophagy
The data implied that the interaction between Beclin1 and Bcl2 could be blocked by MA
Summary
Maslinic acid, abbreviated from 2α, 3β-dihydroxyolean-12-en-28-oic acid, MA, a member of triterpenes (Figure 1), is widely found in nature and is mainly present in olive-pomace oil (an olive skin wax), being the principal component of the wax-like coating in the olive skin [1]. MA was reported to exhibit anti-tumor [2], antioxidant activities [3], have antiallodynic and analgesic effects [4], and anti-inflammation [5], anti-virus [6], parasitostatic effects [7]. Apoptosis is involved in the mechanism of action by which MA suppresses the viability of a wide range of cancers [12] by regulating many downstream signaling pathways that are activated through PKC receptors [14]. The involved pathways include the p38 MAPK/mitochondria/caspase pathway [11, 12] and NF kappa B signaling pathway [2]. Www.impactjournals.com/oncotarget the exact working target of MA in cancer cells requires further investigation
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