{'fraction_non_alphanumeric': 0.03301476976542137, 'fraction_numerical': 0.03388357949609035, 'mean_word_length': 4.619512195121951, '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}}
[Role of ERK/FoxO3a signal axis in inhibitory effect of vitexin 1 (VB-1) in HepG2 cell proliferation].

OBJECTIVE
To investigate whether the ERK/FoxO3a signal axis could induce the inhibitory effect of vitexin 1 (VB-1) in HepG2 cell proliferation.


METHOD
The MTT method was adopted to observe the effect of different concentrations of VB-1 on human hepatoma carcinoma cell line HepG2 and immortalized human embryo liver cell line L-02. The cell growth was assessed by the clone formation assay. The protein phosphorylation levels of ERK1/2 and FoxO3a were measured by the western blot.


RESULT
VB-1 inhibited the viability of HepG2 cell line in a concentration-dependent manner, with a weak effect on L-02 cell line. VB-1 could effectively inhibit the anchorage-dependent growth of HepG2 cells, and reduce the expression levels of pERK1/2 and pFoxO3a in a concentration-dependent manner. MEK1/2 inhibitor PD98059 could enhance VB-1' s effect in inhibiting HepG2 cell proliferation and ERK1/2, FoxO3a phosphorylation.


CONCLUSION
VB-1 inhibits the proliferative activity of hepatoma carcinoma cell line HepG2 by blocking the ERK/FoxO3a signal axis.