ABSTRACT
BACKGROUND: Breast cancer is a heterogeneous disease that has various clinical outcomes. Bax-interacting factor-1 (Bif-1) is a member of the endophilin B family that generates the pro-apoptotic BCL2-Associated X (BAX) protein in response to apoptotic signals. Lack of Bif-1 inhibits the intrinsic pathway of apoptosis and enhancements the risk of tumor genesis. The present study aimed to investigate the relationship between hormone receptors (ER, PR, and HER2) status and different levels of Bif-1 gene expression in breast cancer patients. METHODS: Bif-1 gene expression was evaluated in 50 breast cancer tumors and 50 normal breast mammary tissues using the SYBR Green real-time RT-PCR technique. Multivariate and univariate analyses were used to appraise the relationship between the prognostic significance of the Bif-1 gene using SPSS software. In this study, the Bif-1 was selected as a candidate for a molecular biomarker and its expression status in breast cancer patients with hormone receptors (ER, RR, and HER2) compared to patients without these hormone receptors. RESULTS: The study showed that the relative expression of the Bif-1 gene in tissues of patients with hormone receptors in breast cancer compared to those without hormone receptors was not statistically significant. The expression levels of the Bif-1 gene in different groups were evaluated for hormone receptor status. No significant relationship was found between the Bif-1 gene expression and hormone receptors (ER, PR, and HER2) (p > 0.05). CONCLUSION: Bif-1 gene expression may be a useful prognostic marker in breast cancer.
Subject(s)
Breast Neoplasms , Humans , Female , Breast Neoplasms/genetics , Breast Neoplasms/metabolism , bcl-2-Associated X Protein/genetics , bcl-2-Associated X Protein/metabolism , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Carrier Proteins , Gene Expression , HormonesABSTRACT
Chlorella vulgaris is a form of microalgae commonly employed as a biological source of oil for biodiesel production. Major algal cultivation strategies are focused on stimulating growth rate and lipid content. In the present study, the algal growth media was supplemented with iron (III) chloride (FeCl3), as a stimulating factor for growth and lipid production, in three iron concentrations including 90, 200, and 500 µM. The turbidity of algal cells was measured on different days, to determine the growth rate. In optimum iron concentration, this measurement experienced a 2.1-fold increase. Next, the lipid content was extracted, and the amount of lipid produced in each treatment was calculated, which demonstrated a 4.57-fold increase in lipid productivity. The expression of genes corresponding to the metabolic enzymes (i.e. acetyl-CoA carboxylase (accD) and ribulose bisphosphate carboxylase large chain (rbcL)) was evaluated using real-time PCR under different initial iron feeds. As demonstrated in the results, the initial iron feed of 90 µM was an optimum concentration that obtained the highest growth rate, more cell density, and increased lipid production. In 90 µM initial iron concentration, the expression of accD and rbcL genes showed a 4.8- and 35-fold increase, respectively, compared to that of the control genes. Based on the results, this optimum iron concentration could satisfy the industrial interest in biodiesel production from C. vulgaris as a potential stimulating factor. However, higher levels of iron (e.g. 200 and 500 µM) failed to act as positive stress for increasing biodiesel production. Finally, in this paper, different mechanisms where iron affects acetyl-CoA carboxylase (ACCase) and 1,5-ribulose bisphosphate carboxylase/oxygenase (RuBisCo) are illustrated.
Subject(s)
Biomass , Chlorella vulgaris/chemistry , Microalgae/genetics , Ribulose-Bisphosphate Carboxylase/genetics , Acetyl-CoA Carboxylase/genetics , Biofuels , Chlorella vulgaris/genetics , Culture Media , Fatty Acids/genetics , Gene Expression Regulation/genetics , Iron/metabolismABSTRACT
Gene silencing can occur either through repression of transcription, termed transcriptional gene silencing (TGS), or through translation repression andmRNA degradation, termed posttranscriptional gene silencing (PTGS). PTGS results from sequence-specific mRNA degradation in the cytoplasm without dramatic changes in transcription of corresponding gene in nucleus. Both TGS and PTGS are used to regulate endogenous genes. Interestingly, mechanisms for gene silencing also protect the genome from transposons and viruses. In this paper, we first review RNAi mechanism and then focus on some of its applications in biomedical research such as treatment for HIV, viral hepatitis, cardiovascular and cerebrovascular diseases, metabolic disease, neurodegenerative disorders and cancer.
