Personalized and Precision Medicine Journal

Abstract Mitochondria are the extra-nuclear source of DNA in cells and play an important role in cell death susceptibility,  oxidative stress regulation, metabolism, and signaling in normal cells. Because of this, its dysfunction can contribute to the progression of cancer and metastasis. Also, mtDNA mutations have been reported in many cancers, followed by altered mitochondrial activity and cellular signaling . This increase in mtDNA mutation is due to the proximity of the genome to the OXPHOS system which are thought to be more in extent than mutation nuclear. These mutations do not inactivate energy metabolism but change its state. Therefore, it is not surprising that the function of mitochondria is vital for cancer cells, in addition to understanding the mechanisms of mitochondrial function in the process of tumor formation and cancer progression is essential for cancer treatments.

Abstract PTEN is a tumor suppressor gene with important roles in apoptosis. This gene is located on chromosome 10q23 and is one of the most frequently inactivated genes in cancers. Severe underexpression of PTEN has been reported in several types of cancer, including endometrial, prostate, breast, and brain cancer. Also, this gene is epigenetically silenced through aberrant hypermethylation of CpG islands on its promoter. The present study investigated the promoter methylation and expression levels of PTEN in patients with Non-Small Cell Lung Carcinoma (NSCLC).
The study included 20 patients with NSCLC, whose bisulfite-treated DNA samples were investigated using the Methyl-Specific PCR (MSP) with primers specific for either methylated or non-methylated forms of PTEN. PTEN expression was also assessed using real-time PCR.
 20 samples from NSCLC patients, 70% (n=14) showed PTEN underexpression, while 85% (n=17) had PTEN promoter methylation. Also, 12 of 17 (70%) samples with PTEN promoter methylation had concomitant PTEN underexpression.
According to our results, there was a significant correlation between the PTEN promoter methylation and NSCLC. PTEN underexpression and promoter methylation were also significantly correlated.

Abstract Hesperidin is a flavanone present in citrus fruits, such as oranges and lemons. It exerts non-toxic activities in normal cells; however, it has been reported to suppress cell proliferation in several cancer types. Moreover, it was shown that dietary hesperidin acts as an anti-carcinogenic agent for some tumors. In the present study, we investigated the effect of hesperidin on breast cancer cell line MCF7 and also its effects on the expression of apoptosis-related genes in this cell line.
MCF7 cells were divided into 4 groups, including 3 study groups and 1 control group. Each study group was treated with 50, 75, or 100 μg/mL hesperidin, while the control group was left untreated. The samples underwent real-time PCR using the primers specific for BCL-2 and BAX, as the study genes, while GAPDH was used as the control.
According to our findings, hesperidin caused a significant decrease in BCL-2 mRNA levels at all the doses used in the study groups compared to the control group (p < 0.002). The observed decrease was dose-dependent. Also, hesperidin induced a significant overexpression of BAX when used in doses of 75 and 100 µg/mL in comparison to the control group.
The present study proved the significant apoptosis-inducing effect of hesperidin on the breast cancer cell line MCF7.

Abstract Nanotechnology involves the creation and manipulation of materials at nanoscale to create products that exhibit novel properties. Nano-TiO2, as one of the top five nanoparticles in annual production, is widely applied in industries ranging from healthcare to drug delivery. The properties of nanoTiO2 have raised concerns regarding toxicity. Annexin V-FITC/PI double staining and a flow cytometer were used to detect apoptosis. A significant increase in apoptosis was observed at concentrations of TiO2-NP of 50-100 µg/ml, varying between 25-40% apoptosis by 24 h. To further investigate the aptotic and toxic effects of these substances, it is recommended that this study be performed in the in vivo phase.

Abstract One of the most well-known side effects of anticancer drugs is the disruption of spermatogenesis. One of the most important causes of infertility in men is impaired spermatogenesis. Busulfan is a cytotoxic alkylating agent and belongs to the alkyl sulfonate group. This agent causes DNA damage by cross-linking with DNA. It kills spermatogonial stem cells. The use of healthy antioxidants can reduce the side effects of alkylating agents. In this study, we measured the protective effect of curcumin on testicular tissue of mice treated with busulfan by measuring BAX expression as an apoptotic inducer and Bcl2 as an apoptotic inhibitor. The expression levels of the two apoptotic regulatory genes Bax and Bcl-2 were evaluated by realtime PCR in four groups of mice (control, treatment with busulfan, treatment with curcumin, and treatment with busulfan + curcumin). It was observed in the busulfan group that bcl2 expression decreased, and Bax increased significantly, and the busulfan + curcumin group showed the opposite effect. Curcumin can be beneficial as a dietary supplement in cancer patients treated with drugs such as busulfan.