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Backgrounds & objectives: Colorectal cancer (CRC) is the third leading cause of cancer death worldwide. Micro RNAs are a group of non-coding small RNAs that inhibit the translation of target mRNA. MiR-146a-5p, as a tumor suppressor, has abnormal expression in many cancers. In this basic research, our goal was to restore the expression level of miR-146a-5p to normal level and to investigate its effect on the expression of the MMP9 gene in HT-29 cells.
Methods: this study evaluates the effect of transfection of miR-146a-5p in HT-29 cell line. At first, the HT-29 cell line from colorectal cancer was cultured in RPMI-1640 culture media and then  were transfected with miR-146a-5p using Jet-PEI reagent. qRT-PCR technique was employed to evaluate the expression level of miR-146a-5p and MMP9 genes. The statistical analysis was performed using GraphPad Prism 6 software.
Results: According to the obtained data, the onset of the invasion and metastasis, in particular, at the final stage of colorectal cancer may be related to a reduction in the expression of miR-146a-5p. The results of the qrRT-PCR test showed that by increasing the expression level of miR-146a-5p in HT-29 cells, the expression level of MMP9 gene decreased in the miR-146a-5p transfected group compared to the control group.
Conclusions: According to this study, activation of metastatic pathways was due to the down regulation of miR146a-5p. Accordingly, miR-146a-5p can inhibits migration of these cells through down-regulating the expression of metastasis-related genes. Hence, miR-146a-5p can be a new diagnostic biomarker and new therapeutic target for CRC.
 

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Background & objectives: Nuclear Factor kappa B (NF-κB), a master switch transcription factor, plays a critical role in the progression and development of hyperglycemia-induced microangiopathy. Hyperglycemia activates NF-κB, and subsequently increases pro-inflammatory cytokines such as TNF-α, IL-6 and IL-1β leading to development of inflammation. Some new studies have revealed the involvement of microRNA-146a (miR-146a) in the pathogenesis of diabetic complications through an NF-κB-dependent negative feedback loop manner. Despite numerous reports indicating changes of plasma miR-146a during hyperglycemia, the origin of this change remains unclear. This study was designed to evaluate the role of NF-κB on the miR-146a gene expression level in human umbilical vein endothelial cells (HUVECs) during a hyperglycemic condition.
Methods: HUVECs were cultured in normal glucose (5 mmol/L), and hyperglycemic (25 mmol/L) endothelial cell growth medium in the six well plates for 24 h. JSH-23 (30 μmol/L), as an inhibitor of NF-κB translocation to the nucleus, was added to the culture medium, 30 min before induction of hyperglycemia. Quantitative Real Time PCR was performed to measure the expression levels of miR-146a and mRNA NF-κB. NF-κB activity was measured by Elisa.
Results: Hyperglycemia markedly increased the NF-κB activity and mRNA level in HUVECs. The expression of miR-146a significantly increased in hyperglycemic group compared to the normoglycemic group. On the other hand, JSH-23 prevented from miR-146a increment in hyperglycemic group and also it increased the mRNA expression level of NF-κB in this group.
Conclusion: This result shows that NF-κB increases the gene expression of miRNA-146a in the early phase of hyperglycemia in HUVECs.