Antitumor effects of curcumin on the proliferation, migration and apoptosis of human colorectal carcinoma HCT‑116 cells

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.

Curcumin sensitizes Epstein‑Barr‑immortalized lymphoblastoid cell lines to inorganic arsenic toxicity

“…In the case of curcumin, its anti-proliferative effects in EBV-immortalized LCLs have been reported to be predominantly exerted through causing G1-phase arrest. However, in cell lines derived from monocytic leukemia and gallbladder, breast and colorectal cancer cells, the phytochemical was observed to induce arrest in S phase (37)(38)(39)(40)(41). In addition, curcumin causes DNA damage in human lymphocytes (42,43) and activates apoptosis with phosphatidylserine exposure, cytochrome C release, poly(ADP-ribose) polymerase (PARP) cleavage and DNA damage in LCLs and EBV-positive B-lymphoma cell lines (17,18,44,45).…”

Anticancer effects of dihydromyricetin on the proliferation, migration, apoptosis and in vivo tumorigenicity of human hepatocellular carcinoma Hep3B cells

“…Cell viability was performed using a colony formation assay [ 22 ]. Hep3B cells were seeded into a 6-well plate (3 × 10 2 cells/well) for 8 h, followed by treatment with two different concentrations of DHM and NDP for 24 h. Hep3B cells were cultured with drug-containing medium for ten days.…”

Curcumin Regulates Cancer Progression: Focus on ncRNAs and Molecular Signaling Pathways

“…Furthermore, curcumin can counteract the increased levels of p-ERK and p-NF-kB (112). Xiang et al, documented that curcumin also can repress the proliferation, migration and apoptosis by regulating the NF-kB signaling pathway in human colorectal carcinoma HCT−116 cells (113). In T47D breast cancer cells, curcumin treatment for 48 h, prevented human autocrine growth hormone (GH) signaling mediated NF-kB activation and miR-183-96-182 cluster stimulated epithelial mesenchymal transition (114).…”