{'fraction_non_alphanumeric': 0.026382978723404255, 'fraction_numerical': 0.01446808510638298, 'mean_word_length': 5.189473684210526, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Anticancer activity of oleiferoside B involving autophagy and apoptosis through increasing ROS release in MCF-7 cells and SMMC-7721 cells

Abstract Oleiferoside B is a triterpenoid monomer compound, mainly isolated from roots of Camellia oleifera Abel, the underlying mechanism of its antitumour is not clear. In the present study, oleiferoside B potently inhibited SMMC-7721 and MCF-7 cells proliferation and cause cells apoptosis. In addition, it activated an autophagy-mediated cell death pathway, as indicated by the accumulated the ratio of LC3- II/LC3- I and inhibited apoptosis protein expression after pre-treatment with autophagy inhibitors 3-MA. Further studies showed that oleiferoside B-induced apoptosis and autophagy was attributed to ROS release. In vivo oleiferoside B (1.0, 0.5 mg/kg) effectively suppressed tumour growth. In conclusion, our finding reveals a novel mechanism of action of oleiferoside B in cancer cells via induction of apoptosis and autophagy through ROS generation. Therefore, our results provided new insight into the mechanism of the antitumour effect of oleiferoside B as a prospective therapeutic drug in the tumour. Graphical Abstract