Cytokines are signalling proteins generated in most part by immune cells that have critical functions in cellular lifespan. Here we present recent data on three selected anti-inflammatory cytokines: interleukin (IL)-10, IL-4 and transforming growth factor  (TGF-). IL-10 inhibits the synthesis of major pro-inflammatory cytokines, chemokines, and mediates anti-inflammatory reactions. IL-4 is a multifunctional cytokine which plays a crucial role in the regulation of immune responses and is involved in processes associated with development and differentiation of lymphocytes and regulation of T cell survival. Transforming TGF-, which in normal cells or pre-cancerous cells, promotes proliferation arrest which represses tumour growth. In this review, we focus on the influence of IL-10, IL-4 and TGF- on various types of cancer as well as potential of these selected cytokines to serve as new biomarkers which can support effective therapies for cancer patients. This article is presented based on a review of the newest research results.

Background: Lycopene, gingerol, and silymarin have a potential anticancer activity in many types of neoplasms. Healthy lifestyle and proper diet are associated with a reduced risk of cancer and other diseases. Increasingly, clinical research focuses on the mechanisms of action of natural compounds and their impact on the development of cancer. The aim of the present study was to determine the effect of lycopene, gingerol, and silymarin on apoptosis, mitochondrial potential and caspase-3/7 activity in the U118-MG cell line. Methods: Human glioblastoma cells were incubated with lycopene, [6]-gingerol, and silymarin for 24 and 48 h. Apoptosis was monitored using the Annexin V labelling, caspase-3/7 activity, and early hallmark of apoptosis were determined with mitochondrial membrane potential changes. Results: Our data showed a significant decrease in the viability glioblastoma cells U118-MG after 48 h treatment with lycopene, [6]-gingerol, and silymarin. Conclusions: Our data could confirm the stimulative effects of used compounds on apoptosis and changes in mitochondrial potential in a dose-dependent manner.