Objective: Identifying the dynamics of prostate tumor aggressiveness is essential to find new therapeutics for the treatment. Cancer stem cells contribute to cancer progression by promoting tumor growth and metastasis, resisting treatment, and evading the immune system. Interleukin 6 (IL-6) is a pleiotropic cytokine that functions in inflammation, immune response, etc. However, dysregulated expression of IL-6 plays a pathological role in such conditions as cancer. In this study, we aimed to elucidate the effect of IL-6 on cancer stemness genes in prostate cancer cells. Methods: Enrichment of stem-like cells was achieved through the formation of tumor spheres using the DU-145 cell line. Sphere formation was conducted in a medium supplemented with IL-6 and compared to a control group. The number of spheres was quantified, and the resulting pellet was collected for quantitative reverse transcription polymerase chain reaction analysis to assess the impact of IL-6 induction on the expression of stemness-related genes. Results: Tumor sphere numbers and sizes increased in IL-6-induced environment. NANOG expression elevated in an IL-6-enriched environment compared to the nontreated spheres. Our results demonstrated that IL-6 induction in prostate tumor spheres upregulates NANOG gene expression. Conclusion: Inducing IL-6 in prostate tumor spheres stimulates stemness biomarker NANOG genes. NANOG may be suggested as a therapeutic target for metastatic prostate cancer. Cite this article as: Seven D, Tecimel D, Bayrak ÖF. NANOG dominates IL-6 induced sphere formation in prostate cancer. Urol Res Pract. 2023;49(6):376-380.

Pancreatic ductal adenocarcinoma (PDAC) pathology is known for its uncontrollable progress due to highly invasive characteristics and refractory behavior against existing chemotherapies. The aberrant expression of CDH1 (expresses the protein E-cadherin) is associated with increased overall survival in various cancers, however, E-cadherin expression in PDAC progression has remained elusive. We investigated the impact of exogenously elevated E-cadherin levels on the tumorigenicity of transduced low grade and metastatic PDAC cell lines, Panc-1 and AsPC-1, respectively. Constitutive expression of E-cadherin promoted a more hybrid E/M state in AsPC-1 cells, while it was associated with the acquisition of a more epithelial-like state in Panc1 cells. Our study suggests that E-cadherin may play differential roles in determining the metastatic characteristics of primary and metastatic pancreatic cancer cells.

Lung adenocarcinoma (LUAD) remains the leading cause of mortality worldwide, while asthma is the most prevalent chronic disease affecting individuals of all ages. The shared airway involvement in these global health concerns results in exposure to common risk factors, suggesting a potential overlap in their genetic background. Given the roles oxidative stress and chronic inflammation play in both LUAD and asthma, we aimed to investigate similarities in their molecular mechanisms and to explore whether these shared transcriptomic signatures may prove useful for potential drug repurposing hypotheses by analyzing relevant transcriptomic datasets. This analysis identified a set of genes and co-expression interactions shared between asthma and LUAD, suggesting potential common molecular mechanisms underlying both diseases. Specifically, DNAJC3, APOBEC3G, and PRDX4 were highlighted as potential common molecular mediators underlying both diseases, offering correlative evidence for shared pathways. These genes may represent key molecular links connecting the pathogenic processes of asthma and LUAD. The transcriptomic profiles of asthma and lung cancer datasets reveal common molecular interactions, suggesting potential shared biological mechanisms between the two diseases. These findings provide a computational framework that may guide future studies investigating therapeutic associations and possible drug–gene relationships in lung adenocarcinoma and asthma.