Aging is a risk factor for various human disorders, including cancer. Current literature advocates that the primary principles of aging depend on the endogenous stress‐induced DNA damage caused by reactive oxygen species 50 Hz low‐frequency magnetic field was suggested to induce DNA damage and chromosomal instability. NF‐kB, activated by DNA damage, is upregulated in age‐related cancers and inhibition of NF‐kB results in aging‐related delayed pathologies. Metformin (Met), an NF‐kB inhibitor, significantly reduces both NF‐kB activation and expression in aging and cancer. This in vitro study, therefore, was set out to assess the effects of 5mT MF in 50 Hz frequency and Met treatment on the viability and proliferation of aged mouse NIH/3T3 fibroblasts and expression of RELA/p65, matrix metalloproteinases MMP2 and MMP9, and E‐cadherin (CDH1) genes. The trypan blue exclusion assay was used to determine cell viability and the BrdU incorporation assay to determine cell proliferation. The MMP‐2/9 protein analysis was carried out by immunocytochemistry, NF‐kB activity by ELISA and the expressions of targeted genes by qRT–PCR methods. Four doses of Met (500 uM, 1 mM, 2 mM and 10 mM) suppressed both the proliferation and viability of fibroblasts exposed to the MF in a dose‐dependent pattern, and the peak inhibition was recorded at the 10 mM dose. Met reduced the expression of NF‐kB, and MMP2/9, elevated CDH1 expression and suppressed NF‐kB activity. These findings suggest that Met treatment suppresses the carcinogenic potential of 50 Hz MFs in aged mouse fibroblasts, possibly through modulation of NF‐kB activation and epithelial‐mesenchymal transition modulation.

Uzun zamandır üzerinde çalıştığımız ‘’Ürolojik Vakalar, Tedaviler Ve Literatürde Yaklaşım’’ kitabını sizlere sunmaktan gurur duymaktayız. Mesleğimiz gereği, her üroloji uzmanı günlük pratikte zorlu vakalarla, nadir görülen vakalarla karşılaşmaktadır. Bu kitap içinde de bölüm yazarlarının günlük pratikte karşılaştıkları vakaları, vakaya yaklaşımlarını ve en güncel bilgiler ışığında ilgili konu başlığında literatür bilgileri sunulmaktadır. Dolayısı ile bu kitap meslektaşlarımıza benzer konular hakkında hızlı ve kolay bilgiye ulaşımı sağlamaktadır.

Objective: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide, characterized by profound metabolic reprogramming and limited therapeutic options. Peroxisomes are essential metabolic organelles involved in lipid metabolism, redox homeostasis, and detoxification, and increasing evidence suggests that peroxisomal dysfunction contributes to tumor progression. However, the role of peroxisome biogenesis–related genes in HCC remains insufficiently characterized. This study aimed to investigate the potential involvement of the peroxisome-related genes PEX16 and DHRS4 in HCC by integrating bioinformatics analyses with experimental validation.Methods: Differential gene expression analyses were performed using the GEO datasets GSE183349 and GSE14945 to identify peroxisome-associated genes altered in HCC. The expression levels of PEX16 and DHRS4 were subsequently validated in vitro using quantitative real-time PCR (qPCR) in the HepG2 hepatocellular carcinoma cell line and HUVEC cells as controls.Results: Bioinformatics analyses revealed that PEX16 and DHRS4 were significantly upregulated in HCC datasets. Consistent with the in silico findings, qPCR analysis demonstrated significantly increased expression of both genes in HepG2 cells compared with HUVEC cells (PEX16: p=0.0021; DHRS4: p=0.038). The integrated in silico and in vitro analyses demonstrate that PEX16 and DHRS4 are consistently upregulated in hepatocellular carcinoma.Conclusions: These findings suggest that both genes may serve as peroxisome-associated molecular biomarkers reflecting metabolic reprogramming in HCC. Further validation in patient-derived samples and functional studies are warranted to evaluate their diagnostic and prognostic potential.

Objective: Hepatocellular carcinoma remains a major contributor to cancer mortality worldwide, with low five-year survival rates despite treatments, underscoring the need for more effective and targeted therapies. Metformin, an oral antihyperglycemic agent, has gained attention for its potential anticancer properties. The present study aims to investigate the effects of metformin on key inflammatory cytokines involved in hepatocellular carcinoma (HCC) progression, as well as on the expression of c-Jun, a key subunit of the AP-1.Method: HepG2 cells were treated with metformin at a range of concentrations from 500 μM to 10 mM for 24 hours. To evaluate the anticancer effects of metformin, cell viability was assessed using the trypan blue exclusion method, while IL-6 and IL-8 concentrations were quantified by ELISA. Furthermore, c-Jun protein expression was examined by immunocytochemistry.Results: Metformin treatment led to a significant reduction in the levels of IL-6 and IL-8 in HepG2 cells compared to control group (p