Background: This study systematically investigates the therapeutic effects of naringenin (NAR) and oleuropein (OLE) on prostate cancer through miR-155-5p regulation. Methods: Experimental studies conducted on MAT-LyLu prostate cancer cell lines revealed that the application of NAR (50 μM) and OLE (75 μM) significantly increased miR-155-5p expression by 2.89-fold and 1.74-fold, respectively (p < 0.05). Bioinformatics analyses have indicated that miR-155-5p interacts with critical oncogenic pathways such as KRAS, CDK2, NF-κB, and TGF-β/Smad2. Computational analyses have revealed that miR-155-5p interacts with 16 critical oncogenic targets, including KRAS and CDK2. Molecular docking studies showed that NAR binds to the Switch I/II region of KRAS with a binding energy of −8.2 kcal/mol, while OLE binds to the ATP-binding pocket of CDK2 with an affinity of −9.1 kcal/mol. Pharmacokinetic evaluations revealed that NAR indicated high oral bioavailability (93.763% HIA) and full compliance with Lipinski’s rules, while OLE required advanced formulation strategies due to its high polarity. Network pharmacology analyses have shown that NAR affects lysosomal functions and enzyme regulation, while OLE affects G protein-coupled receptors and oxidoreductase activity. Results: Results indicate that NAR and OLE exhibit antitumor effects through multiple mechanisms by increasing miR-155-5p expression and inhibiting critical oncogenic targets in prostate cancer. Conclusions: Findings suggest that the dietary intake of these natural compounds (citrus and olive products) should be considered in prostate cancer prevention strategies, shedding light on the epigenetic mechanisms of polyphenols in cancer treatment and contributing to the development of new therapeutic strategies.

Olive leaf tea (OLT), rich in phenolics, exhibits antioxidant, anti-inflammatory, and potential anticancer effects; however, the in vivo efficacy remains unclear. This study evaluated the chemopreventive and systemic effects of OLT in a murine Ehrlich Ascites Tumor (EAT) model, with a focus on the treatment timing. OLT was prepared by aqueous infusion and characterized for total phenolic content (TPC: 25.74 mg GAE/g), DPPH scavenging (197.88 µmol TE/g), FRAP activity (81.23 µmol Fe²⁺/g), and LC-MS/MS profile (oleuropein 77.6%). Mice received OLT orally before or after tumor inoculation. Prophylactic OLT reduced EAT cell counts (from 31.48 × 10⁷ to 21.15 × 10⁷), ascites volume (from 4.58 to 2.98 mL), elevated miR-155-5p (14.34-fold), normalized ALT/AST, and restored hepatic antioxidants without histopathological damage. Co-treatment with 5-FU preserved efficacy while reducing hepatotoxicity. In conclusion, OLT provides timing-dependent anticancer and systemic protective effects in the EAT model, supporting its potential as a cost-effective nutraceutical for cancer prevention and adjunctive therapy.

Breast cancer remains one of the most prevalent types of cancer among women globally, contributing significantly to cancer-related mortality. Despite advancements in treatment, many cases continue to exhibit resistance to chemotherapy, radiotherapy, and hormonal therapies, often resulting in drug resistance, high recurrence rates, and severe side effects. Consequently, the role of the natural food components in cancer prevention and treatment is gaining increasing attention in modern medicine. This study focuses on quercetin, a phytochemical compound, and its effects on the breast cancer cell line MCF-7. Specifically, the study has investigated changes in the expression of miR-15a and miR-34a—microRNAs (miRNAs) known to regulate gene expression at the post-transcriptional level—and the P53 gene, which is critically involved in apoptosis. The analysis was performed using quantitative polymerase chain reaction (qPCR) and Western blot techniques. The results demonstrated that quercetin treatment at concentrations of 40 µM and 80 µM led to a 1.34-fold and 2.73-fold increase in P53 gene expression, respectively. Additionally, the tumor suppressor miRNA miR-15a showed expression changes of 1.48-fold and 1.69-fold at the same quercetin concentrations. Similarly, miR-34a expression levels increased by 1.23-fold and 1.39-fold at 40 µM and 80 µM, respectively. These findings suggest that dietary phytochemicals, such as quercetin, may have therapeutic potential by modulating miRNA expression and targeting the p53 pathway. In conclusion, quercetin emerges as a promising natural therapeutic agent for breast cancer, warranting further in vivo studies and clinical trials to confirm its efficacy and explore its potential as a part of combination therapies.