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The slow advance in anticancer drug development can be attributed to the limitations of conventional models, predominantly monolayer cell (2D) cultures and animal models, which inadequately recapitulate the complex nature of human malignant tumors. Three-dimensional (3D) in vitro models are invaluable tools in drug screening; however, creating a universal model for all cancer types poses challenges due to the diverse nature of cancers. The aim of this work was to develop a single, versatile model using alginate microfibers to accommodate cultivation of various cancer cells.

Osteosarcoma (OS) is a highly aggressive primary malignant bone tumor that most commonly affects children, adolescents, and young adults. The standard treatment for OS consists of surgical resection and chemotherapy, whereas radiation therapy is recommended for the unresectable tumor. Due to its easy metastasis and recurrence, the 5-year overall survival rate is only 66.5 %. Thus, there is a critical need to recognize the molecular mechanisms underlying OS development and pathogenesis. Traditionally, two-dimensional (2D) cells are widely used in cancer biology and pre-clinical studies. However, 2D models are unable to mimic cell–cell and cell-extracellular matrix interactions which are crucial for adequate cellular function. Three-dimensional (3D) model systems are able to recapitulate key features of human cancer and are recognized as a promising platform for fundamental and translational research. In the present work, we established an osteosarcoma 3D model based on alginate microbeads and studied the effect of combined treatment with doxorubicin (Doxo), widely used chemotherapeutic, and quercetin (Quer), a plant pigment with anticancer properties, on OS model systems.

Brain trauma leads to the induction of neural stem cell proliferation and the migration of young neurons to injured areas. However, these neurons are insufficient to fully restore neuronal function due to the limited potential of adult neurogenesis. This study aimed to investigate the effect of hypoxia, a condition that underlines a wide spectrum of brain pathologies, on pluripotency and the capacity of stem cells to differentiate into neural progenitors. We analyzed the expression of SOX genes and microRNAs as they control a variety of cellular processes during neuronal differentiation, including cell proliferation and cell fate determination. In vitro neuronal differentiation of human embryonal carcinoma cell line NT2/D1 and induced pluripotent stem cells were used as a model system of adult neurogenesis. Cobalt chloride was used to induce hypoxia. The results of the analysis showed that, following hypoxia, the efficiency of neuronal induction was significantly decreased, that coincident with decline in mRNA expression levels of SOXB and SOXC genes. In contrast to that, the expression level of miR-21 was significantly increased. Our findings advance the study of SOX TFs, miR-21, and their possible interplay in ischemia-related pathologies, establishing them as prospective biomarkers and possible targets for future diagnostic and therapeutic approaches.

Introduction: Prolonged exposure to sunlight, has a harmful effect on skin cells encompassing reduced viability, morphological changes, and altered gene expression. The two most prevalent types ofskin cancer,squamous cell carcinoma (cSCC) and basal cell carcinoma (BCC), arise from malignant transformation of keratinocytes. UV radiation, among other factors, serves as the primary cause of these tumors. Previous data hasshown that changesin different SOX genes expression in these cancer types correlates with disease progression, suggesting their role as oncogenes/tumor suppressors. The presented work is focused on examining the impact of UVB radiation on the expression of SOX2 and SOX9 genesin HaCaT cells derived from human keratinocytes. Methods: Using a custom-made UV solarsimulator for the irradiation of HaCaT cells with 150 mJ/cm2 or 300 mJ/cm2 , we analyzed SOX2 and SOX9 gene expression. In order to determine the protective effects of quercetin, anti-inflammatory bioflavonoid, we treated irradiated HaCaT with quercetin, and analyzed SOX gene expression. Results: Our resultsindicate that UVB radiation induces a dose dependent decrease of SOX2 expression while expression of SOX9 was increased at the dose of 150 mJ/cm2 in HaCaT. Treatment of cells with quercetin increased the expression of both SOX2 and SOX9 genesin HaCaT cellsfollowing UVB radiation at both doses compared to irradiated cells. Conclusions: Further research is needed to understand the molecular mechanisms and significance of SOX2 and SOX9 in UVB-induced cellular responses, in the context of nonmelanoma cancers with potential implications for targeted therapeutic strategies for nonmelanoma cancers