Inflammatory bowel disease (IBD) as a chronic inflammation in colon and small intestine has two subtypes: ulcerative colitis (UC) and Crohn’s disease (CD). Genome studies have shown that UC and CD are related to microRNAs (miRNAs) expression in addition to environmental factors. This article reviews important researches that have recently been done on miRNAs roles in CD and UC disease. First, miRNA is introduced and its biogenesis and function are discussed. Afterward, roles of miRNAs in inflammatory processes involved in IBD are showed. Finally, this review proposes some circulating and tissue-specific miRNAs, which are useful for CD and UC fast diagnosis and grade prediction. As a conclusion, miRNAs are efficient diagnostic molecules especially in IBD subtypes discrimination and can be used by microarray and real time PCR methods for disease detection and classification.

Background: Deregulation of the EGFR signaling pathway activity has been shown to can be effective in resistance to EGFR-TKIs, such as Tarceva (erlotinib), in glioblastoma cells. In addition, reports have shown that the reduction of miRNA-7 expression levels is associated with an increase in the expression of EGFR. Here, we evaluated the effect of miRNA-7 on EGFR expression and sensitivity of the U373-MG glioblastoma to erlotinib. Methods: The effect of miRNA-7 on EGFR expression was examined using RT-qPCR and western blotting. Trypan blue and MTT assays were performed to explore the effect of treatments on cell growth and survival, respectively. The combination index analysis was used to evaluate the interaction between drugs. Apoptosis was measured by ELISA cell death assay. Results: We showed that miRNA-7 markedly inhibited the expression of EGFR and decreased the growth of glioblastoma cells, relative to blank control and negative control miRNA (p < 0.05). Introduction of miRNA-7 synergistically increased the sensitivity of the U373-MG cells to erlotinib. Results of apoptosis assay demonstrated that miRNA-7 can trigger apoptosis and enhance the erlotinib-mediated apoptosis. Conclusions: Our results show that miRNA-7 plays a critical role in the growth, survival and sensitivity of the U373-MG cells to erlotinib by targeting EGFR. Thus, miRNA-7 replacement therapy can become an effective therapeutic procedure in glioblastoma.

Objectives Down‐regulation of miRNA‐7 is correlated with over‐expression of IRS‐1 and IRS‐2 proteins, the upstream regulators of IGF‐1R/Akt pathway, in glioblastoma cells. In this study, the effect of miRNA‐7 on expression of IRS‐1 and IRS‐2 and sensitivity of the U373‐MG glioblastoma cells to erlotinib was explored. Methods After miRNA‐7 transfection, the expression of IRS‐1 and IRS‐2 mRNAs was measured by RT‐qPCR. Trypan blue assay was used to assess the effect of miRNA‐7 on cell proliferation. The effects of miRNA‐7 and erlotinib, alone and in combination, on cell survival and apoptosis were measured using MTT assay and ELISA cell death assay, respectively. Key findings Our data showed that miRNA‐7 markedly inhibited the expression of IRS‐1 and IRS‐2 in a time‐dependent manner, inhibited the proliferation of glioblastoma cells and enhanced apoptosis (P < 0.05, relative to control). Pretreatment with miRNA‐7 synergistically inhibited the cell survival rate and decreased the IC50 of erlotinib. Furthermore, miRNA‐7 significantly augmented the apoptotic effect of erlotinib. Conclusions Our data propose that inhibition of IRS‐1 and IRS‐2 by miRNA‐7 can effectively induce apoptosis and sensitize glioblastoma cell to EGFR‐TKIs. Therefore, miRNA‐7 may be a potential therapeutic target in patients with glioblastoma.

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Treatment of neurological disorders has always been one of the challenges with which scientists are faced due to poor prognosis and symptom overlap, as well as the progress of the disease process. Neurological disorders such as Huntington’s, Parkinson's, Alzheimer's diseases, and Amyotrophic Lateral Sclerosis are very debilitating. Therefore, finding a biomarker is essential for early diagnosis and treatment goals. Recent studies have focused more on molecular factors and gene manipulation to find effective diagnostic and therapeutic biomarkers. Among these factors, microRNAs (miRNAs/miRs) have attracted a lot of attention. On the other hand, a growing correlation between miRNAs and neurological disorders has caused scientists to consider it as a diagnostic and therapeutic target. In this line, the miR-153 is one of the important and highly conserved miRNAs in mice and humans, whose expression level is altered in neurological disorders and also improves neurogenesis. MiR-153 can regulate multiple biological processes by targeting various factors. Furthermore, miR-153 expression also can be regulated by important regulators, such as long non-coding RNAs (e.g., KCNQ1OT1), and some compounds (e.g., Tanshinone IIA), altering the expression of miR-153. Given the growing interest in miR-153 as a biomarker and therapeutic target for neurological diseases as well as the lack of comprehensive investigation of miR-153 function in these disorders, it is necessary to identify the downstream and upstream targets and also it's potential as a therapeutic biomarker target. In this review, we will discuss the critical role of miR-153 in neurological disorders for novel diagnostic and prognostic purposes, and also its role in multi-drug resistance.