Last update 01 Nov 2024

miR-1

Last update 01 Nov 2024

Basic Info

Synonyms

fibronectin type III and SPRY domain containing 1, Fibronectin type III and SPRY domain-containing protein 1, FSD1

+ [5]

Introduction

May be involved in microtubule organization and stabilization.

Drugs associated with miR-1

ML316

Target

miR-1

Mechanism

miR-1 inhibitors

Active Org.

Whitehead Institute for Biomedical Research

Originator Org.

Whitehead Institute for Biomedical Research

Active Indication

Mycoses

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with miR-1

100 Translational Medicine associated with miR-1

0 Patents (Medical) associated with miR-1

1,270

Literatures (Medical) associated with miR-1

01 Oct 2024·American Journal of Reproductive Immunology

Quantitative Modeling to Characterize Maternal Inflammatory Response of Histologic Chorioamnionitis in Placental Membranes

Article

Author: Sandepudi, Kirtana ; Chou, Teresa ; Goldstein, Jeffery A. ; Cooper, Lee A. ; Patel, Payal V. ; Senkow, Karolina J. ; Nguyen, Megan B.

ABSTRACTProblemThe placental membranes are a key barrier to fetal and uterine infection. Inflammation of the membranes, diagnosed as maternal inflammatory response (MIR) or alternatively as acute chorioamnionitis, is associated with adverse maternal‐fetal outcomes. MIR is staged 1–3, with higher stages indicating more hazardous inflammation. However, the diagnosis relies upon subjective evaluation and has not been deeply characterized. The goal of this work is to develop a cell classifier for eight placental membrane cells and quantitatively characterize MIR1–2.Method of StudyHematoxylin and eosin (H&E)‐stained placental membrane slides were digitized. A convolutional neural network was trained on a dataset of hand‐annotated and machine learning‐identified cells. Overall cell class‐level metrics were calculated. The model was applied to 20 control, 20 MIR1, and 23 MIR2 placental membrane cases. MIR cell composition and neutrophil distribution were assessed via density and Ripley's cross K‐function. Clinical data were compared to neutrophil density and distribution.ResultsThe classification model achieved a test‐set accuracy of 0.845, with high precision and recall for amniocytes, decidual cells, endothelial cells, and trophoblasts. Using this model to classify 53 073 cells from healthy and MIR1–2 placental membranes, we found that (1) MIR1–2 have higher neutrophil density and fewer decidual cells and trophoblasts, (2) Neutrophils colocalize heavily around decidual cells in healthy placental membranes and around trophoblasts in MIR1, (3) Neutrophil density impacts distribution in MIR, and (4) Neutrophil metrics correlate with features of clinical chorioamnionitis.ConclusionsThis paper introduces cell classification into the placental membranes and quantifies cell composition and neutrophil spatial distributions in MIR.

01 Oct 2024·Cancer Reports

Activating Invasion and Metastasis in Small Cell Lung Cancer: Role of the Tumour Immune Microenvironment and Mechanisms of Vasculogenesis, Epithelial‐Mesenchymal Transition, Cell Migration, and Organ Tropism

Review

Author: He, Carl

ABSTRACTBackgroundSmall cell lung cancer (SCLC) harbours the most aggressive phenotype of all lung cancers to correlate with its bleak prognosis. The aggression of SCLC is partially attributable to its strong metastatic tendencies. The biological processes facilitating the metastasis in SCLC are still poorly understood and garnering a deeper understanding of these processes may enable the exploration of additional targets against this cancer hallmark in the treatment of SCLC.Recent FindingsThis narrative review will discuss the proposed molecular mechanisms by which the cancer hallmark of activating invasion and metastasis is featured in SCLC through important steps of the metastatic pathway, and address the various molecular targets that may be considered for therapeutic intervention. The tumour immune microenvironment plays an important role in facilitating immunotherapy resistance, whilst the poor infiltration of natural killer cells in particular fosters a pro‐metastatic environment in SCLC. SCLC vasculogenesis is achieved through VEGF expression and vascular mimicry, and epithelial‐mesenchymal transition is facilitated by the expression of the transcriptional repressors of E‐cadherin, the suppression of the Notch signalling pathway and tumour heterogeneity. Nuclear factor I/B, selectin and B1 integrin hold important roles in SCLC migration, whilst various molecular markers are expressed by SCLC to assist organ‐specific homing during metastasis. The review will also discuss a recent article observing miR‐1 mRNA upregulation as a potential therapeutic option in targeting the metastatic activity of SCLC.ConclusionTreatment of SCLC remains a clinical challenge due to its recalcitrant and aggressive nature. Amongst the many hallmarks used by SCLC to enable its aggressive behaviour, that of its ability to invade surrounding tissue and metastasise is particularly notable and understanding the molecular mechanisms in SCLC metastasis can identify therapeutic targets to attenuate SCLC aggression and improve mortality.

20 Aug 2024·Journal of Virology

AcMNPV-miR-2 affects Autographa californica nucleopolyhedrovirus infection by regulating the expression of ac28 and several other viral early genes

Article

Author: Duan, Zhuowen ; Yu, Xinghua ; Wang, Jinwen ; Teng, Tingkai

ABSTRACT Virus-encoded microRNAs (miRNAs) exert diverse regulatory roles in the biological processes of both viruses and hosts. This study delves into the functions of AcMNPV-miR-2, an early miRNA encoded by Autographa californica multiple nucleopolyhedrovirus (AcMNPV). AcMNPV-miR-2 targets viral early genes ac28 ( lef-6 ), ac37 ( lef-11 ), ac49 , and ac63 . Overexpression of AcMNPV-miR-2 leads to reduced production of infectious budded virions (BVs) and diminished viral DNA replication. Delayed polyhedron formation was observed through light and transmission electron microscopy, and the larval lifespan extended in oral infection assays. Moreover, the mRNA expression levels of two Lepidoptera-specific immune-related proteins, Gloverin and Spod-11-tox, significantly decreased. These findings indicate that AcMNPV-miR-2 restrains viral load, reducing host immune sensitivity. This beneficial effect enables the virus to combat host defense mechanisms and reside within the host for an extended duration. IMPORTANCEVirus-encoded miRNAs have been extensively studied for their pivotal roles in finetuning viral infections. Baculoviruses, highly pathogenic in insects, remain underexplored concerning their encoded miRNAs. Previous reports outlined three AcMNPV-encoded miRNAs, AcMNPV-miR-1, -miR-3, and -miR-4. This study delves into the functions of another AcMNPV-encoded miRNA, AcMNPV-miR-2 (Ac-miR-2). Through a comprehensive analysis of target gene expression, the impact on larvae, and variations in host immune-related gene expression, we elucidate a functional pathway for Ac-miR-2. This miRNA suppresses viral load and infectivity and prolongs lifespans of infected larva by downregulating specific viral early genes and host immune-related genes. These mechanisms ultimately serve the virus's primary goal of enhanced propagation. Our study significantly contributes to understanding of the intricate regulatory mechanisms of virus-encoded miRNAs in baculovirus infections.

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miR-1

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