Drug delivery systems based on the zeolitic imidazolate framework ZIF-8 have recently attracted viable research interest owing to their capability of decomposing in acidic media and thus performing targeted drug delivery. In vivo realization of this mechanism faces a challenge of relatively slow decomposition rates, even at elevated acidic conditions that are barely achievable in diseased tissues. In this study we propose to combine drug delivery nanocomposites with a semiconductor photocatalytic agent that would be capable of inducing a local pH gradient in response to external electromagnetic radiation. In order to test this principle, a model drug-releasing nanocomposite comprising photocatalytic titania nanotubes, ZIF-8, and the antitumor drug doxorubicin has been investigated. This system was demonstrated to release the drug in a quantity sufficient for effectively suppressing IMR-32 neuroblastoma cells that were used as a model diseased tissue. With locally applied UV irradiation, this result was achieved within 40 minutes, which is a relatively short time compared to the release duration in systems without photocatalyst, typically taking from several hours to several days.

The p53 protein is crucial for regulating cell survival and apoptosis in response to DNA damage. However, its influence on therapy effectiveness is controversial: when DNA damage is high p53 directs cells toward apoptosis, while under moderate genotoxic stress it saves the cells from death and promote DNA repair. Furthermore, these processes are influenced by the metabolism of transition metals, particularly copper since they serve as cofactors for critical enzymes. The metallochaperone Atox1 is under intensive study in this context because it serves as transcription factor allegedly mediating described effects of copper. Investigating the interaction between p53 and Atox1 could provide insights into tumor cell survival and potential therapeutic applications in oncology. This study explores the relationship between p53 and Atox1 in HCT116 and A549 cell lines with wild type and knockout TP53. The study found an inverse correlation between Atox1 and p53 at the transcriptional and translational levels in response to genotoxic stress. Atox1 expression decreased with increased p53 activity, while cells with inactive p53 had significantly higher levels of Atox1. Suppression of both genes increased apoptosis, while suppression of the ATOX1 gene prevented apoptosis even under the treatment with chemotherapeutic drugs. The findings suggest that Atox1 may act as one of key elements in promotion of cell cycle under DNA-damaging conditions, while p53 works as an antagonist by inhibiting Atox1. Understanding of this relationship could help identify potential targets in cell signaling pathways to enhance the effectiveness of combined antitumor therapy, especially in tumors with mutant or inactive p53.

A planar memristor was fabricated by a hybrid method combining AFM patterning and inkjet printing.

Survival mechanisms are activated in tumor cells in response to therapeutic ionizing radiation. This reduces a treatments effectiveness. The p53, p63, and p73 proteins belonging to the family of proteins that regulate the numerous pathways of intracellular signal transduction play a key role in the development of radioresistance. This review analyzes the p53-dependent and p53-independent mechanisms involved in overcoming the resistance of tumor cells to radiation exposure.