Crocin has pharmacological effects against the pathological behavior of colon cancer cells by interacting with the STAT3 signaling pathway.

The aim of the present study was to investigate changes in proliferation, apoptosis, inflammation and chemokine release of colon cancer cells after treatment with crocin, as well as to investigate the signaling pathway that is regulated by crocin. The inhibition rates of different doses of crocin on the proliferation of HCT116 cells were measured by MTT assay. The IC₅₀ was calculated from the inhibition rates at 48 h. Proliferation curves of HCT116 cells were plotted after treatment with 271.18 µM (high-dose group) or 135.6 µM (low-dose group) crocin. Flow cytometry and Hoechst 33342/propidium iodide double staining were used for detecting apoptosis. ELISA was used to measure the levels of macrophage inflammatory protein 2, interleukin (IL)-8, monocyte chemoattractant protein 1, tumor necrosis factor-α, IL-6 and IL-1β in the supernatant from cultured HCT116 cells following both high- and low-dose crocin treatment. Phosphorylated (P)-STAT3/STAT3 in HCT116 cells were measured by western blotting. Crocin inhibited the proliferation of HCT116 cells in a dose-dependent manner and the high-dose treatment with crocin resulted in a lower rate of proliferation. Additionally, crocin increased the apoptosis of HCT116 cells and the high-dose treatment with crocin led to a higher level of apoptosis. Notably, crocin decreased the secretion of chemokines and inflammatory factors from HCT116 cells and the high-dose treatment with crocin caused the greatest reduction in secretion of the factors. Crocin reduced the ratio of P-STAT3/STAT3, and thereby reduced the release of cytokines. The present study demonstrated that crocin may have pharmacological effects against the pathological behavior of colon cancer cells, and its mechanism of action may be related to the STAT3 signaling pathway.