Fibromodulin (FMOD) is known as one of very important extracellular matrix small leucine-rich proteoglycans. This small leucine-rich proteoglycan has critical roles in the extracellular matrix organization and necessary for repairing of tissue in many organs. Given that the major task of FMOD is the modulation of collagen fibrillogenesis. However, recently observed that FMOD plays very important roles in the modulation of a variety of pivotal biological processes including angiogenesis, regulation of TGF-β activity, and differentiation of human fibroblasts into pluripotent cells, inflammatory mechanisms, apoptosis and metastatic related phenotypes. Besides these roles, FMOD has been considered as a new tumor-related antigen in some malignancies such as lymphoma, leukemia, and leiomyoma. Taken together, these findings proposed that FMOD could be introduced as diagnostic and therapeutic biomarkers in treatment of various cancers. Herein, for first time, we highlighted the various roles of FMOD in the cancerous conditions. Moreover, we summarized the diagnostic and therapeutic applications of FMOD in cancer therapy.

Metastasis is known to be one of the important factors associated with cancer-related deaths worldwide. Several cellular and molecular targets are involved in the metastasis process. Among these targets, matrix metalloproteinases (MMPs) play central roles in promoting cancer metastasis. MMPs could contribute toward tumor growth, angiogenesis, migration, and invasion via degradation of the extracellular matrix and activation of pre-pro-growth factors. Therefore, identification of various cellular and molecular pathways that affect MMPs could contribute toward a better understanding of the metastatic pathways involved in various tumors. Micro-RNAs are important targets that could affect MMPs. Multiple lines of evidence have indicated that deregulation of various micro-RNAs, including miR-9, Let-7, miR-10b, and miR-15b, affects metastasis of tumor cells via targeting MMPs.

Background and aimVitiligo is a chronic skin disease characterized by a total or partial loss of melanocytes from the epidermis and other tissues of the skin. It is placed in the class of secondary psychiatric disorders and can also lead to psychological problems. The main aim of this study was to assess social acceptance in vitiligo patients.MethodsThis cross-sectional study was conducted on all of the patients (n=150) with vitiligo who were referred to dermatology clinics in Rafsanjan, Iran. The patients completed a social acceptability questionnaire (Marlowe–Crowne Social Desirability Scale), and information regarding their demographic characteristics was also collected. Data were gathered and analyzed with descriptive and inferential statistics using SPSS-19 software.ResultsThe mean age of the patients was 27.56±10.53 years and 65.9% were female. Mean score of social acceptance among the patients was 13.51±7.08. The results showed that the mean scores of social acceptance were significantly lower in women, in those with single marital status, in those with face and neck lesions, and in those with disease duration less than 5 years.ConclusionThe results showed that certain groups of patients with vitiligo are at greater risk of experiencing lower social acceptance.

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder, which is associated with impairments of memory, thinking, language, and reasoning. Despite extensive research aiming at the treatment of AD, durable and complete remissions are rare. Hence, new therapeutic approaches are required. Among various therapeutic approaches, stem cells (ie, neural stem cells, mesenchymal stem cells, and embryonic stem cells) and delivery of protective genes such as encoding nerve growth factor, APOE, and glial cell-derived neurotrophic factor have generated promise in AD therapy. Here, we summarized a variety of effective therapeutic approaches (ie, stem cells, and genes) in AD therapy.

BackgroundAlpha-synuclein (SNCA) as the presynaptic protein is expressed in different tissues and prevents insulin-resistance (IR) through increasing glucose-uptake by adipocytes and muscles. However, the effect of insulin metabolism on SNCA expression has scarcely elucidated. In present study we assessed the probable effect of insulin resistance on SNCA expression in muscle C2C12 cells and also skeletal muscle tissues of type 2 diabetic mice.Materials and methodsSixteen male C57BL/6 mice were divided into two experimental groups, including control and type 2 diabetic mice with IR (induced by high-fat diet + low-dose streptozotocin). The animals of the study involved the measurements of fasting blood glucose, oral-glucose-tolerance-test, as well as fasting plasma insulin. Moreover, insulin-resistant and insulin-sensitive muscle C2C12 cells were prepared. The insulin-resistance was confirmed by the glucose-uptake assay. Comparative quantitative real time PCR was used to assess the SNCA expression.ResultsThe obtained results have showed a significant ~ 27% decrease in SNCA expression level in muscle tissue of diabetic mice (P = 0.022). Moreover, there was a significant change of SNCA expression in insulin-resistant C2C12 cells (P < 0.001).ConclusionType 2 diabetes due to insulin-resistance can decrease SNCA gene expression in muscles. In addition to the role of SNCA in cell susceptibility to insulin and glucose uptake, the SNCA expression can also be affected by insulin metabolism.

Breast cancer is the most prevalent cancers worldwide and causes a significant amount of deaths annually. Spalt-like transcription factor 4 is known as a transcription factor, which has an important role in the proliferation of cancerous cells. Small interfering RNA (siRNA) is a short-chain molecule of 20 to 25 nucleotides that protrude on two sides of the 3′, two nucleotides. In this study, using a specific sequence of siRNA against the sequence of this gene, its activity is investigated in the cell line of breast cancer. The breast cancer cells (MCF-7) were cultured and then, using a specific anti-sal-like 4 (SALL4) siRNA, their toxic doses were determined. Then, the gene is transfected into the cell. Proliferation and expression of the SALL4 and BCL-2 gene were measured using the real-time polymerase chain reaction method. The specific concentration of siRNA IC 50 of the SALL4 gene was 40.35 nmole. Gene expression results indicated that the expression of the Bcl-2 gene in the siRNA group was significantly reduced (P < 0.05). SiRNA can increase the apoptosis of breast cancer cells by reducing the gene expression of SALL4 gene and Bcl-2; it can be used as a novel targeted therapy. This strategy, in addition to increasing the specificity of the drug, also reduces the side effects when compared with conventional chemotherapy. K E Y W O R D S biomarker, breast cancer, diagnosis, spalt-like transcription factor 4 | INTRODUCTIONBreast cancer is accounted as the most common malignancy in women worldwide. Breast cancer can be affected by a wide range of internal and external factors and is also characterized by molecular heterogeneity 1,2 and drug resistance is the major obstacle for its successful chemotherapy. 3 Despite various existing screening programs and new therapeutic strategies including gene therapy, 4,5 cell therapy, 6-13 and using a new generation of drug delivery systems 14-21 finding and developing new diagnostic and therapeutic approaches in the treatment of various cancers such as breast cancer are required. [22][23][24][25][26][27] To enhance the therapeutic efficacy of breast cancer, it is imperative to understand profoundly the molecular pathogenesis of cancer cells as well as identify newer candidate genes/proteins, which are crucial in the proliferating and J Cell Biochem. 2019;120:9392-9399. wileyonlinelibrary.com/journal/jcb 9392 |

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