MicroRNAs (miRNAs) are endogenous ∼23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.

MicroRNAs: Target Recognition and Regulatory Functions

Among deregulated microRNAs (miRs) in human malignancies, miR-221 has been widely investigated for its oncogenic role and as a promising biomarker. Moreover, recent evidence suggests miR-221 as a fine-tuner of chronic liver injury and inflammation-related events. Available information also supports the potential of miR-221 silencing as promising therapeutic intervention. In this systematic review, we selected papers from the principal databases (PubMed, MedLine, Medscape, ASCO, ESMO) between January 2012 and December 2020, using the keywords "miR-221" and the specific keywords related to the most important hematologic and solid malignancies, and some non-malignant diseases, to define and characterize deregulated miR-221 as a valuable therapeutic target in the modern vision of molecular medicine. We found a major role of miR-221 in this view. 

http://www.cell.com/article/S2162253122000336/pdf

miR-221/222 as biomarkers and targets for therapeutic intervention on cancer and other diseases: A systematic review

The prognosis of acute myeloid leukemia (AML) remains a challenge. In this study, we applied the weighted gene coexpression network analysis (WGCNA) to find survival-specific genes in AML based on 42 adult CN-AML samples from The Cancer Genome Atlas (TCGA) database. Eighteen hub genes (ABCA13, ANXA3, ARG1, BTNL8, C11orf42, CEACAM1, CEACAM3, CHI3L1, CRISP2, CYP4F3, GPR84, HP, LTF, MMP8, OLR1, PADI2, RGL4, and RILPL1) were found to be related to AML patient survival time. We then compared the hub gene expression levels between AML peripheral blood (PB) samples (n = 162) and control healthy whole blood samples (n = 337). Seventeen of the hub genes showed lower expression levels in AML PB samples. The gene expression analysis was also done among AML BM (bone marrow) samples of different stages: diagnosis (n = 142), posttreatment (n = 42), and recurrent (n = 12) stages. The results showed a significant increase of ANXA3, CEACM1, RGL4, RILPL1, and HP in posttreatment samples compared to diagnosis and/or recurrent samples. Transcription factor (TF) prediction of the hub genes suggested LTF as the top hit, overlapping 10 hub genes, while LTF itself is just one of the hub genes. Also, 3671 correlation links were shown between 128 mRNAs and 209 lncRNAs found in survival time-related modules. Generally, we identified candidate mRNA biomarkers based on CN-AML data which can be extensively used in AML prognosis. In addition, we mapped their potential regulatory mechanisms with correlated lncRNAs, providing new insights into potential targets for therapies in AML.

Identification of Survival-Related Genes in Acute Myeloid Leukemia (AML) Based on Cytogenetically Normal AML Samples Using Weighted Gene Coexpression Network Analysis

Trehalose, as a food and feed additive, can regulate physiological and pathological processes by activating autophagy, yet the molecular mechanism of trehalose dominated a rise in autophagy has not been elucidated. This study investigated the mechanisms of trehalose-induced autophagy in porcine granulosa cells (PGCs). Trehalose was internalized into PGCs by endocytosis and caused a temporary change of the lysosome pH, ultimately inducing autophagy. Furthermore, miRNA-seq analysis of PGCs indicated that trehalose upregulated the expression of miR-221-5p_R-4, which can target nuclear receptor binding factor 2 (NRBF2) to induce autophagy of PGCs. In summary, this study reveals that miR-221-5p_R-4 targeting NRBF2 was involved in the autophagy of PGCs challenged by trehalose, which was taken up by PGCs through endocytosis. 

miR-221-5p_R-4 regulates internalized trehalose-induced autophagy by targeting NRBF2 in porcine granulosa cells

Porcine respiratory and reproductive syndrome (PRRS) is one of the most devastating infectious diseases of pigs, causing reproductive failures in sows and severe respiratory symptoms in piglets and growing pigs. MicroRNAs (miRNAs) are reported to play an essential role in virus-host interactions. In this study, we demonstrated that miR-451 enhanced type I interferon (IFN-I) production through targeting proteasome subunit β8 (PSMB8), therefore restricting PRRS virus (PRRSV) replication. We showed that the expression of PSMB8 was upregulated by PRRSV infection, and knockdown of PSMB8 inhibited PRRSV replication by promoting IFN-I production. Moreover, we demonstrated that PSMB8 interacted with the regulatory domain of IRF3 to mediate K48-linked polyubiquitination and degradation of IRF3. Also, importantly, we showed that PSMB8, as a target gene of miR-451, negatively regulated IFN-I production by promoting IRF3 degradation, which is a previously unknown mechanism for PSMB8 to modulate innate immune responses. 

miR-451-targeted PSMB8 promotes PRRSV infection by degrading IRF3

Background Long non-coding RNA (lncRNA) has gradually received widespread attention due to its role in regulating tumor progression. However, in renal cell cancer (RCC), the exact function of lncRNA LINC00671 remains uncertain. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for detecting LINC00671 and miR-221-5p expressions in RCC tissues and cell lines. Western blotting technique was utilized for detecting the expressions of epithelial-mesenchymal transition (EMT)-associated proteins (E-cadherin and N-cadherin) and suppressor of cytokine signaling 1 (SOCS1). The correlation between clinicopathological features and LINC00671 expression was also evaluated. RCC cell multiplication, migration and invasion were measured by CCK-8, EdU and Transwell assays, respectively. The targeted relationships between LINC00671 as well as the SOCS1 3'UTR and miR-221-5p were verified by RNA immunoprecipitation (RIP) and luciferase reporter gene assay. Results LINC00671 expression in RCC tissues and cells was significantly reduced. Patients with low LINC00671 expression had relatively shorter disease-free survival and overall survival. Moreover, LINC00671 expression was linked to lymph node metastasis, tumor stage, and tumor size. In Caki-1 and 769-P cell lines, LINC00671 overexpression restrained the multiplication, migration, invasion, as well as the EMT process of RCC cells in vitro. In terms of mechanism, miR-221-5p was identified as a target of LINC00671, and LINC00671 could up-regulate SOCS1 by repressing miR-221-5p. Conclusion LINC00671 regulates the miR-221-5p/SOCS1 axis as a tumor suppressor in RCC.

LINC00671 inhibits renal cell cancer progression via regulating miR-221-5p/SOCS1 axis.

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LINC00671 inhibits renal cell cancer progression via regulating miR-221-5p/SOCS1 axis.