The effect of interleukin 12 on lung cancer cells

Nowadays, stem cell therapies are one of the therapeutic methods used in many areas of medicine. Although different treatment methods have been developed, there is no cure for cancer. Lung cancer is the most common type of cancer. Many experimental studies have reported the therapeutic and protective properties of mesenchymal stem cells (MSCs), while in cancer models it has been shown to suppress and stop the proliferation of cancer cells. However, in some studies, it has been shown that stem cells stimulate the formation of cancer, increase the mass, cause new vessel formation and invasion of cancer. Communication between MSCs and cancer cells is provided by the help of cytokines secreted from the cells. The therapeutic properties of MSCs are mediated by these cytokines. The aim of this study was to keep MSCs and A549 lung cancer cells in vitro in the same medium, to ensure that MSCs secrete interloukin (IL)-12 from cytokines that suppress the growth of cancer cells. To investigate the effects of IL-12 on genes in apoptotic and autophagic pathways in A549 cancer cells, as well as their effects on cell cycle and proliferation genes, to see the effect of MSCs on cancer cells. This study was carried out by forming 3 different groups at cell culture level and in 6 different time zones. IL-12p70 and IL-12p40 levels from cytokines released from cells were determined by ELISA from the collected media. In addition, IL-12 subunits and receptors, apoptosis and autophagy, cell cycle markers and proliferation markers were investigated by real time polymerase chain reaction (rt-PZR). As a result of our ELISA test and gz-PCR, resistance to apoptosis may have started to develop in the first hours when IL-12 is secreted, and this apoptotic resistance may be regressed with IL-12 effect in the later hours and the cell cycle time may be decreased after IL-12 release. phase is thought to extend. When the proliferation markers of mRNA expression with real time PCR were examined, it was observed that IL-12 decreased after secretion and then started to be expressed again slowly. In conclusion, MSCs were found to be insufficient when used alone to suppress A549 cancer cells by IL-12 release, but could not be stopped despite the suppression of proliferation of cancer cells by IL-12 release.