{'fraction_non_alphanumeric': 0.018274111675126905, 'fraction_numerical': 0.017258883248730966, 'mean_word_length': 5.444444444444445, '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}}
Molecular mechanism of silymarin-induced apoptosis in a highly metastatic lung cancer cell line anip973.

BACKGROUND
Silymarin, the main flavonoid constituent element extracted from Silybum marianum possessing antioxidant activity, is already known to be able to block the NF-κB activation process and result in cell apoptosis, implicating silymarin's potential to control cancer cell growth.


MATERIALS AND METHODS
In this study, based upon the above assumption, silymarin was administered to a highly metastatic lung cancer cell line Anip973 to test silymarin's role in cancer cell proliferation.


RESULTS
Silymarin had significant inhibitory effects on the proliferation of Anip973 cells in a dose-dependent and time-response manner within 48 hours. Silymarin can induce Anip973 apoptosis.


CONCLUSIONS
Silymarin may in vitro inhibit the proliferation of the human lung adenocarcinoma cell line Anip973 and induce apoptosis via the mitochondria-dependent caspase cascade pathway.