Abstract
Curcumin is the main component of the Chinese herbal plant turmeric, which has been demonstrated to possess antitumor and other pharmacological properties. The aim of the present study was to investigate the effects of curcumin on the viability, migration and apoptosis of human colorectal carcinoma HCT‑116 cells, and to explore the underlying molecular mechanisms. In addition, it was investigated whether the antitumor effect of curcumin on HCT‑116 cells could match that of the chemotherapeutic drug 5‑fluorouracil (5‑FU). HCT‑116 cells were treated with curcumin (10, 20 and 30 µM) and 5‑FU (500 µM), and cell viability and proliferation were detected by Cell Counting Kit‑8 and colony formation assays, respectively. The migration and invasion of treated cells were determined using Transwell and carboxyfluorescein succinimidyl amino ester fluorescent labeling assays. Cell cycle distribution and apoptosis rates were detected by flow cytometry. Furthermore, cell morphology changes associated with apoptosis were observed by fluorescence microscopy with acridine orange/ethidium bromide dual staining. To investigate the possible underlying molecular mechanisms, the gene and protein levels of Fas, Fas‑associated via death domain (FADD), caspase‑8, caspase‑3, matrix metalloproteinase (MMP)‑9, nuclear factor (NF)‑κB, E‑cadherin and claudin‑3 were detected using quantitative PCR analysis, zymography and western blotting. The results revealed that curcumin markedly inhibited the viability and proliferation of HCT‑116 cells in a dose‑ and time‑dependent manner. The migration, aggregation and invasion of HCT‑116 cells into the lungs of mice were decreased by curcumin treatment in a dose‑dependent manner. S‑phase arrest and gradually increased apoptotic rates of HCT‑116 cells were observed with increasing curcumin concentrations. Additionally, the mRNA and protein levels of apoptosis‑associated proteins (Fas, FADD, caspase‑8 and caspase‑3) and E‑cadherin in HCT‑116 cells were upregulated following treatment with curcumin in a dose‑dependent manner. By contrast, the expression of migration‑associated proteins, including MMP‑9, NF‑κB and claudin‑3, was downregulated with increasing curcumin concentrations. These data suggested that the inhibitory effect of curcumin on HCT‑116 cells may match that of 5‑FU. Therefore, curcumin induced cell apoptosis and inhibited tumor cell metastasis by regulating the NF‑κB signaling pathway, and its therapeutic effect may be comparable to that of 5‑FU.