期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 16, 期 1, 页码 1544-1561出版社
MDPI
DOI: 10.3390/ijms16011544
关键词
autophagy; autophagosome; apoptosis; crocin; colorectal cancer; p53
资金
- Emirates Foundation [2009-079]
- National Research Foundation [U-IRCA 2012-21832]
- UPAR
- Terry Fox Foundation
Crocin, a bioactive molecule of saffron, inhibited proliferation of both HCT116 wild-type and HCT116 p53-/- cell lines at a concentration of 10 mM. Flow cytometric analysis of cell cycle distribution revealed that there was an accumulation of HCT116 wild-type cells in G1 (55.9%, 56.1%) compared to the control (30.4%) after 24 and 48 h of crocin treatment, respectively. However, crocin induced only mild G2 arrest in HCT116 p53-/- after 24 h. Crocin induced inefficient autophagy in HCT116 p53-/- cells, where crocin induced the formation of LC3-II, which was combined with a decrease in the protein levels of Beclin 1 and Atg7 and no clear p62 degradation. Autophagosome formation was not detected in HCT116 p53-/- after crocin treatment predicting a nonfunctional autophagosome formation. There was a significant increase of p62 after treating the cells with Bafilomycin A1 (Baf) and crocin compared to crocin exposure alone. Annexin V staining showed that Baf-pretreatment enhanced the induction of apoptosis in HCT116 wild-type cells. Baf-exposed HCT116 p53-/- cells did not, however, show any enhancement
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