Cyanidin-3-O-glucoside (C3G), an active ingredient in anthocyanins, mainly exists in dark cereals. C3G was investigated for its effect on human gastric cancer (GC) cells, together with its molecular mechanism. The CCK-8 assay results showed that C3G had significant antiproliferative effects on GC cells, but it had little effect on normal cells. Western blot and flow cytometry results showed that C3G regulated the reduction of mitochondrial membrane potential and arrested the cell cycle in the G2/M phase through the AKT signaling pathway, causing the cells to undergo apoptosis. Additionally, in MKN-45 cells, C3G markedly raised intracellular reactive oxygen species (ROS) levels. The wound healing assay and Transwell assay results showed that MKN-45 cell migration was significantly inhibited. Western blot results showed that the expression of E-cadherin protein was upregulated and the expressions of β-catenin, N-cadherin, and Vimentin were downregulated. Additionally, following N-acetylcysteine treatment, the expression levels of these proteins were reduced. In conclusion, C3G caused MKN-45 cells to undergo apoptosis; arrested the cell cycle in the G2/M phase; hindered cell migration; and activated the MAPK, STAT3, and NF-κB signaling pathways, by inducing an increase in ROS levels. Thus, C3G may be a promising new medication for the treatment of GC.

Isoorientin (ISO) is a flavonoid compound containing a luteolin structure, which can induce autophagy in some tumor cells. This study investigated the impact of ISO in gastric cancer AGS cells, and performed an experimental analysis on the main signaling pathways and transduction pathways it regulates. CCK–8 assay results showed that ISO reduced the survival rate of gastric cancer AGS cells, but the toxicity to normal cells was minimal. Hoechst 33342/PI double staining assay results showed that ISO induced apoptosis in gastric cancer AGS cells. Further analysis by flow cytometry and Western blot showed that ISO induced apoptosis via a mitochondria-dependent pathway. In addition, the level of reactive oxygen species (ROS) in gastric cancer AGS cells also increased with the extension of the ISO treatment time. However, cell apoptosis was inhibited by preconditioning cells with N–acetylcysteine (NAC). Moreover, ISO arrested the cell cycle at the G2/M phase by increasing intracellular ROS levels. Cell migration assay results showed that ISO inhibited cell migration by inhibiting the expression of p–AKT, p–GSK–3β, and β–catenin and was also related to the accumulation of ROS. These results suggest that ISO-induced cell apoptosis by ROS–mediated MAPK/STAT3/NF–κB signaling pathways inhibited cell migration by regulating the AKT/GSK–3β/β–catenin signaling pathway in gastric cancer AGS cells.

Atractylodin (ATR) has anticancer effects on some tumor cells by inducing apoptosis, but its mechanism in lung cancer remains unclear. This study investigates the inhibitory effect of ATR on A549 lung cancer cells. Cell viability was detected by the Cell Counting Kit-8 assay, and results showed that ATR could significantly inhibit the proliferation of A549 cells. Apoptosis was detected by Annexin V-FITC/PI staining, and apoptosis rate and mitochondrial membrane potential were detected by flow cytometry. Results showed that the effect of ATR on the apoptosis of A549 cells was negatively correlated with the change in mitochondrial membrane potential. Western blot analysis showed that ATR regulated apoptosis induced by mitogen-activated protein kinase, signal transducer and activator of transcription 3, and nuclear factor kappa B signaling pathways. Analyses of reactive oxygen species (ROS), cell cycle, and cell migration showed that ATR induced intracellular ROS accumulation as an initiation signal to induce cell cycle arrest regulated by the AKT signaling pathway and cell migration inhibition regulated by the Wnt signaling pathway. Results showed that ATR can inhibit cell proliferation, induce cell apoptosis, induce cell cycle arrest, and inhibit the migration of A549 cells (p < 0.05 was considered statistically significant, * p < 0.05, ** p < 0.01 and *** p < 0.001).

Tumors pose a serious threat to global public health and are usually treated from two aspects: tumor cells and tumor microenvironment. Compared with traditional chemotherapy drugs, traditional Chinese medicine (TCM) monomers have advantages in tumor treatment, such as multiple targets, multiple levels and synergistic intervention. However, most TCM active ingredients have disadvantages such as poor water solubility and stability, which restrict their clinical application. Nano drug delivery systems have the functions of improving the bioavailability of TCM anti-tumor active ingredients, enhancing tissue targeting, achieving controlled drug release, and inhibiting tumor multidrug resistance. Compared with free monomers, they have higher therapeutic effects and fewer side effects. This article summarizes five commonly used anti-tumor TCM monomer nanocarriers, including lipid nanomaterials, exosomes, polymer micelles, carbon nanotubes, and dendrimers, and explains their anti-tumor mechanisms after combining with TCM, such as inhibiting tumor cell proliferation and metastasis, regulating tumor microenvironment, etc. At the same time, the potential of nano drug delivery systems combined with radiotherapy and immunotherapy is discussed, as well as the current problems of potential toxicity, long-term stability, and complex amplification process, as well as future development directions, aiming to provide a reference for promoting the clinical application of nano drug delivery systems for TCM anti-tumor active ingredients.

Marine collagen peptides (MCPs) are natural products prepared by hydrolyzing marine collagen protein through a variety of chemical methods or enzymes. MCPs have a range of structures and biological activities and are widely present in marine species. MCPs also have a small molecular weight, are easily modified, and absorbed by the body. These properties have attracted great interest from researchers studying antioxidant, anti-tumor, and anti-aging activities. MCPs of specific molecular weights have significant anti-tumor activity and no toxic side effects. Thus, MCPs have the potential use as anti-cancer adjuvant drugs. Free radicals produced by oxidation are closely related to human aging, cancer, arteriosclerosis, and other diseases, but their relationship with cancer is not well known. In this review, we focus on the antioxidant properties of MCPs in the treatment of cancer, highlighting their antioxidant molecular structure and potential for clinical practice.