Chlorogenic acid induces apoptosis and cell-cycle arrest in colorectal cancer cells.

BACKGROUND: Apoptotic agents from natural products like phenolic compounds can be used effectively in the treatment of cancer. Chlorogenic acid (CGA) is one of the phenolic compounds in medicinal plants with anti-cancer properties. In this research, we aimed to explore the anti-cancer mode of action of CGA on colorectal cancer (CRC) cells in vitro conditions. METHODS: HT-29 and HEK-293 cells were cultured after MTT assay for 24 h with CGA 100 µM, and without CGA. Then, flow cytometry assays and the expression of apoptosis-related genes including caspase 3 and 9, Bcl-2 and Bax, and cell cycle-related genes including P21, P53 and NF-κB at mRNA and protein levels were examined. Finally, we measured the amount of intracellular reactive oxygen species (ROS). RESULTS: The cell viability of all two-cell lines decreased in a dose-dependent manner. Moreover, CGA induces cell cycle arrest in HT-29 cells by increasing the expression of P21 and P53. It also induces apoptosis in HT-29 cells by mitigating Bcl-2 and NF-κB expression and elevating caspase 3 and 9 expression and ROS levels. CONCLUSIONS: Considering the cytotoxicity and cell cycle arrest and induction of apoptosis in the colon cancer cell line by CGA, it can be concluded that CGA is a suitable option for the treatment of colon cancer.

Superparamagnetic Iron Oxide Nanoparticles Induce Apoptosis in HT-29 Cells by Stimulating Oxidative Stress and Damaging DNA.

Nanoparticles have garnered considerable scientific attention in recent years due to their diagnostic and therapeutic applications in cancer. The purpose of this study was to determine the effect of superparamagnetic iron oxide nanoparticles (Fe3O4 MNPs) on the induction of apoptosis in human colorectal adenocarcinoma cell line (HT-29) cells. The purpose of this study was to elucidate the mechanisms of apoptosis induced by Fe3O4 MNPs following MTT assay and to determine the optimal dose of 2.5 g/mL for inducing apoptosis in HT-29 cells. In HT-29 cells, Fe3O4 MNPs increased reactive oxygen species (ROS), calcium ion (Ca2+), and DNA damage. Additionally, the Fe3O4 MNPs significantly increased caspase 3 and 9 expression and decreased Bcl-2 expression at the protein and mRNA levels when compared to the control group (P = 0.0001). Fe3O4 MNPs also induced apoptosis in cancer cells by increasing the level of (ROS) and intracellular Ca2+, followed by an increase in caspase 3 and 9 expression and a decrease in Bcl-2 expression and direct DNA damage. Fe3O4 MNPs are an appropriate choice for colon cancer treatment based on their cell toxicity and induction of apoptosis in HT29 cells.

Correction to: Variation in Blood and Colorectal Epithelia's Key Trace Elements along with Expression of Mismatch Repair Proteins from Localized and Metastatic Colorectal Cancer Patients.

The original version of this article unfortunately contained a mistake. The name of "Ali Ghorbani Ranjbary" is now corrected in the author group of this article. The original article has been corrected.

Variation in Blood and Colorectal Epithelia's Key Trace Elements Along with Expression of Mismatch Repair Proteins from Localized and Metastatic Colorectal Cancer Patients.

Colorectal cancer (CRC) is an increasingly common medical issue affecting millions worldwide, and contribution of the body's trace elements to CRC is arguable. The concentrations and buffered status of selenium, iron, copper, zinc, and phosphorus in blood and large intestinal tissues of CRC patients are, respectively, variable and vital for cell physiology. The aim of this study was to assess selenium, iron, copper, zinc, and phosphorus variations in blood and colorectal epithelia along with examining the expression of mismatch repair proteins in CRC patients with/without metastasis for potential diagnosis/therapy. Concentrations of selenium, iron, copper, zinc, and phosphorus in blood of healthy versus CRC patients and colorectal epithelia (adenocarcinomatous versus non-adenocarcinomatous/control) were measured in 40 CRC patients (55.87 ± 11.9 years old) with/without metastasis before surgery using ICP-OES. Mismatch repair (MMR) protein expression was analyzed through histopathological/immunohistochemistry assays, which was sparse in 5 CRC patient's colorectal tissues (12%). Compared with healthy individuals, blood and colorectal tissue's levels of phosphorus, copper, and iron were significantly higher in the CRC patients, and more pronounced in metastatic CRC patients; conversely, blood and colorectal tissue's selenium levels were significantly lower in metastatic patients. Unlike blood zinc, cancerous colorectal tissue's zinc concentration was significantly lower in CRC patients compared to healthy control cohorts. There was no significant difference on the measured elements in samples from CRC patients with MMR- compared to CRC patients with MMR+. Receiver operating characteristic analysis revealed a correlation of blood iron, zinc, copper, and phosphorus to CRC, and inappropriately low levels of blood and colorectal selenium correlated with exacerbated metastasis. Altered levels of selenium, iron, copper, zinc, and phosphorus in vivo may impact the pathogenesis and detection of CRC, and their diagnostic/therapeutic potential in CRC would be revealing.