Abstract 37P
Background
Interleukin-1β (IL-1β) is an inflammatory cytokine; however, in the tumor microenvironment it exhibits pro-oncogenic properties, inducing angiogenesis, metastasis, and local immunosuppression. In this regard, various approaches to the use of IL-1β inhibitors in cancer patients are being considered. However, such treatment should be based on knowledge of cytokine expression in tumor tissue and local immune status.
Methods
For the experiments we used a human alveolar basal epithelial adenocarcinoma cell line (A549) incubated in a full culture medium DMEM (Paneco, Russia) supplemented with 10 mM HEPES-Na, 2 mM glutamine, 10% fetal bovine serum and 1% penicillin, streptomycin, IL-1β solution, and cytostatic drug solution. After 24 hours of incubation IL-1β was added to the cells with a final concentration of 1 ng/ml in the well. After 24 hours, a cytostatic drug was added to some of the cells, the final concentration in the well was 50 μM. The control line were A549 cells without additional treatment. After 24 hours MTT assay was performed to assess the total cellular metabolic activity as an indicator of viability, proliferation and cytotoxicity. The study was carried out with the support of RFBR grants 20-015-00498 and 21-515-10007.
Results
Under the influence of IL-1β the degree of mitochondrial activity in lung cancer cells decreased relative to the control by 34.73%, when exposed to a cytostatic drug - by 42.99%, in the presence of IL-1β and a cytostatic drug - by 45.05%.
Conclusions
According to the MTT test the presence of IL-1β contributed to a decrease in mitochondrial activity in tumor cells, which was enhanced by the action of a cytostatic agent. Possibly, IL-1β of 1 ng/ml with a short incubation time has an antitumor effect, which enhances the efficacy of cytostatics. The results obtained might confirm the importance of the timely initiation of chemotherapy, when pro-inflammatory processes prevail in the tumor microenvironment, and a personalized approach when choosing additional treatment methods.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
RFBR grants 20-015-00498 and 21-515-10007.
Disclosure
All authors have declared no conflicts of interest.