Prostate cancer (PC) is the second most common malignancy among men worldwide and remains a leading cause of cancer-related mortality, highlighting the need for novel molecular tools for diagnosis and targeted therapy. In this study, five DNA aptamers (AptaP1–AptaP5) generated by Cell-SELEX against the LNCaP prostate cancer cell line were characterized for their structural features, tumor recognition, and biological activity. Secondary structure prediction and thermodynamic stability were evaluated in silico. Aptamer recognition was evaluated by flow cytometry in prostate cancer cell lines and by complementary aptafluorescence analyses in both cell lines and a prostate tissue microarray (TMA), while functional effects were evaluated by assessment of metabolic activity and proliferation assays. The selected aptamers preferentially recognized LNCaP and DU145 cells over RWPE-1, whereas no tumor-selective binding was observed for PC3 cells. Aptafluorescence analyses in the prostate TMA demonstrated differential tissue recognition, with signals detected across both primary and metastatic prostate cancer specimens. Moreover, all aptamers significantly reduced metabolic activity and proliferation in prostate cancer cells after 48 h of treatment. Collectively, these findings characterized novel DNA aptamers with promising potential as tools for prostate cancer detection and provide a basis for further investigation of their binding properties and biological effects in clinically relevant models.

Cancer patients are highly vulnerable to severe COVID-19, requiring models that capture tumor–virus interactions. We investigated tumor- and variant-specific effects of SARS-CoV-2 Gamma and Delta infections using patient-derived organoids (PDOs) from metastatic breast, lung, and colorectal cancers. Viral infection was quantified by Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR) 24 h post-infection, and morphological changes and immune mediators were profiled. Genomic analysis using whole-exome sequencing was performed to identify contributing host-related gene alterations. The Delta variant produced consistently higher viral loads in lung and breast PDOs, while colorectal PDOs showed variable susceptibility. Infection led to reduced area and perimeter and increased circularity across all tumor types. Immune profiling revealed distinct responses: Gamma decreased Interferon alpha (IFNα) in lung PDOs and increased E-selectin in colorectal PDOs. Delta broadly reduced inflammatory mediators in lung [10 kDa interferon gamma-induced protein (IP-10) and Intercellular adhesion molecule 1 (ICAM-1)] and breast [Interleukin-6 (IL-6), Interleukin-13 (IL-13), and Interleukin-17A (IL-17A)] PDOs, while increasing Macrophage inflammatory protein 1-beta (MIP-1β) in colorectal PDOs. Host gene variants involved in trafficking (FYCO1 and RAB7A) and immune signaling (FOXA2, SFTPD, STAT3, and TET2) were associated with differential infection profiles. These findings show that SARS-CoV-2 induces variant- and tumor-specific morphological and immunological changes in cancer PDOs, highlighting the potential of this model to unravel host–virus interactions and identify genetic factors that shape infection outcomes in cancer.