BACKGROUND: Micro RNA-126 is known to enhance apoptotic processes and also plays a role in vascular growth through the regulation of vascular endothelial growth factor-mediated signaling, angiogenesis, and vascular integrity. OBJECTIVES: We aimed to determine the role of miR-126 in breast cancer cell lines with a variety of different characteristics to evaluate its interaction with certain cancer-related molecules and mechanisms. METHODS: To determine the effect of presence and absence of miR-126 in MCF-7 and MDA-MB-231 breast cancer cells, miR-126 mimics and inhibitor were transfected. miRNA and gene expressions were observed by using RT-PCR. Viability, proliferation, adhesion, invasion and lateral motility assays were performed to determine cell behavior changes. RESULTS: miR-126 is more effective on MDA-MB-231 cells on cell behavior. We observed an increase in miR-126 expression when miR-126 mimics was transfected to MCF-7 and MDA-MB-231 cells. Also, there was a decrease in miR-126 expression when MCF-7 and MDA-MB-231 cells were transfected with miR-126 inhibitor. Furthermore, presence and absence of miR-126 modulated the gene expressions of VEGF/PI3K/AKT and MAPK signaling in MCF-7 and MDA-MB-231. CONCLUSION: Our study showed that miR-126 is in a state of interaction with a multitude molecules playing a role in breast cancer. According to obtained data, we can say that miR-126 may be more effective in inhibition of metastatic breast cancer (Tab. 4, Fig. 3, Ref. 46). Text in PDF www.elis.sk.

Hepatocellular carcinoma is one of the most prevalent cancers, with a high morbidity rate, even in developed countries. In the present study, the curative effect of the Schiff base (SB) heterodinuclear copper(II)Mn(II) complex on diethylnitrosamine (DEN)-induced liver carcinoma was investigated. Hepatocarcinoma was initiated by an injection of DEN and promoted by phenobarbital (0.05%) in the diet. In addition, the potential nephrotoxicity of SB was evaluated in a cisplatin-induced nephrotoxicity model. Rats were administered the SB complex (1 and 2 mg/kg body weight/day) for 24 weeks, and cancer progression was investigated by macroscopic, histopathological, and western blot examinations. The administration of SB decreased the incidence and the number of hepatic nodules in a dose-dependent manner by regulating inflammation response and the apoptotic pathway. Western blot analyses from the livers of rats treated with SB after DEN induction showed significantly enhanced Bax and caspase-3 levels, with a marked decrease in the levels of Bcl-2, NF-κB p65 and cyclooxygenase (COX)-2. Results from the nephrotoxicity study showed that, whereas cisplatin increased serum urea nitrogen and creatinine levels, no increase in serum biochemical parameters was detected in SB-treated animals. Moreover, protein levels of NF-E2-related factor-2 (Nrf2) and heme oxygenase-1 were lower, whereas nuclear factor-κB (NF-κB p65) and activator protein-1 levels were higher in the kidneys of cisplatin-treated animals compared with that of the SB groups. Therefore, the SB complex could be an alternative chemotherapeutic option for liver cancer treatment once its safety in clinical applications has been examined.

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Human endometrial stem cells (hESCs) are mesenchymal stem cells, which are responsible for the monthly renewal of the basal layer of the human endometrium by facilitating stromal and vascular regeneration. In this study, hESCs were isolated by using three different isolation methods including nonenzymatic and enzymatic digestion with trypsin and collagenase type 1. To determine the efficiency of these three methods, cells were characterized using a cell proliferation assay and mesenchymal and hematopoietic stem cell markers. Our results demonstrate that although the nonenzymatic isolation method gave rise to hESCs that had a higher proliferative rate, the mesenchymal stem cell profiles for hESCs isolated with three methods were similar, with no significant difference for the early passages. However, late passage hESCs isolated using trypsin showed a CD31 high CD44 low profile. Similarly, when hESCs isolated with the nonenzymatic method were kept until late passage, they demonstrated a CD31 high profile with a significant decrease in CD90, CD73, CD44, and CD105 surface expression levels. Only hESCs isolated with collagenase type 1 did not present a significant shift in their mesenchymal CD marker profile from early to late passages, suggesting that the long-term maintenance of mesenchymal markers could only be achieved in cell isolation with collagenase type 1.

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