Microglia and astrocytes maintain tissue homeostasis in the nervous system. Both microglia and astrocytes have pro-inflammatory phenotype and anti-inflammatory phenotype. Activated microglia and activated astrocytes can contribute to several neurological diseases. Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), two groups of non-coding RNAs (ncRNAs), can function as competing endogenous RNAs (ceRNAs) to impair the microRNA (miRNA) inhibition on targeted messenger RNAs (mRNAs). LncRNAs and circRNAs are involved in various neurological disorders. In this review, we summarized that lncRNAs and circRNAs participate in microglia dysfunction, astrocyte dysfunction, neuron damage, and inflammation. Thereby, lncRNAs and circRNAs can positively or negatively regulate neurological diseases, including spinal cord injury (SCI), traumatic brain injury (TBI), ischemia-reperfusion injury (IRI), stroke, neuropathic pain, epilepsy, Parkinson's disease (PD), multiple sclerosis (MS), and Alzheimer's disease (AD). Besides, we also found a lncRNA/circRNA-miRNA-mRNA regulatory network in microglia and astrocyte mediated neurological diseases. Through this review, we hope to cast light on the regulatory mechanisms of lncRNAs and circRNAs in microglia and astrocyte mediated neurological diseases and provide new insights for neurological disease treatment.

/pdf/long-non-coding-rnas-and-circular-rnas-insights-into-36yw6vmxus.pdf

Long Non-coding RNAs and Circular RNAs: Insights Into Microglia and Astrocyte Mediated Neurological Diseases.

LncRNAs have emerged as important regulatory molecules in biological processes. They serve as regulators of gene expression pathways through interactions with proteins, RNA, and DNA. LncRNA expression is altered in several diseases of the central nervous system (CNS), such as neurodegenerative disorders, stroke, trauma, and infection. More recently, it has become clear that lncRNAs contribute to regulating both pro-inflammatory and anti-inflammatory pathways in the CNS. In this review, we discuss the molecular pathways involved in the expression of lncRNAs, their role and mechanism of action during gene regulation, cellular functions, and use of lncRNAs as therapeutic targets during neuroinflammation in CNS disorders.

The Expanding Regulatory Mechanisms and Cellular Functions of Long Non-coding RNAs (lncRNAs) in Neuroinflammation

DNA double strand breaks and cancer

Abstract Emerging evidence indicates that resolution of inflammation is a critical and dynamic endogenous process for host tissues defending against external invasive pathogens or internal tissue injury. It has long been known that autoimmune diseases and chronic inflammatory disorders are characterized by dysregulated immune responses, leading to excessive and uncontrol tissue inflammation. The dysregulation of epigenetic alterations including DNA methylation, posttranslational modifications to histone proteins, and noncoding RNA expression has been implicated in a host of inflammatory disorders and the immune system. The inflammatory response is considered as a critical trigger of epigenetic alterations that in turn intercede inflammatory actions. Thus, understanding the molecular mechanism that dictates the outcome of targeting epigenetic regulators for inflammatory disease is required for inflammation resolution. In this article, we elucidate the critical role of the nuclear factor‐κB signaling pathway, JAK/STAT signaling pathway, and the NLRP3 inflammasome in chronic inflammatory diseases. And we formulate the relationship between inflammation, coronavirus disease 2019, and human cancers. Additionally, we review the mechanism of epigenetic modifications involved in inflammation and innate immune cells. All that matters is that we propose and discuss the rejuvenation potential of interventions that target epigenetic regulators and regulatory mechanisms for chronic inflammation‐associated diseases to improve therapeutic outcomes.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/mco2.173

Targeting epigenetic regulators for inflammation: Mechanisms and intervention therapy

Glioblastoma (GBM) is the most prevalent and deadly primary brain tumor type, with a discouragingly low survival rate and few effective treatments. An important function of the EGFR signalling pathway in the development of GBM is to affect tumor proliferation, persistence, and treatment resistance. Advances in molecular biology in the last several years have shown how important ncRNAs are for controlling a wide range of biological activities, including cancer progression and development. NcRNAs have become important post-transcriptional regulators of gene expression, and they may affect the EGFR pathway by either directly targeting EGFR or by modifying important transcription factors and downstream signalling molecules. The EGFR pathway is aberrantly activated in response to the dysregulation of certain ncRNAs, which has been linked to GBM carcinogenesis, treatment resistance, and unfavourable patient outcomes. We review the literature on miRNAs, circRNAs and lncRNAs that are implicated in the regulation of EGFR signalling in GBM, discussing their mechanisms of action, interactions with the signalling pathway, and implications for GBM therapy. Furthermore, we explore the potential of ncRNA-based strategies to overcome resistance to EGFR-targeted therapies, including the use of ncRNA mimics or inhibitors to modulate the activity of key regulators within the pathway. 

Exploring ncRNA-mediated regulation of EGFR signalling in glioblastoma: From mechanisms to therapeutics.

Design, synthesis, and biological evaluation of tetrahydroisoquinoline based hydroxamate derivatives as HDAC 6 inhibitors for cancer therapy

To maintain genome stability cells have evolved complex DNA repair pathways to correct DNA damage caused by exogenous and endogenous factors. The role of proteins and small non coding RNAs in DNA repair is well known. Recently, several long non coding RNAs (lncRNAs) have emer ged as critical players in regulating DNA double strand break repair by Homologous Recombination (HR) and Non Homologous End Joining (NHEJ). LncRNAs interact with regulatory proteins or coding and other non-coding transcripts involved in DNA repair to modulate DNA repair. This review summarizes the role of lncRNAs in DNA repair by HR and NHEJ pathways.

/pdf/linc-ing-rna-to-dna-repair-1rygzcvdp4.pdf

Linc‘ing’ RNA to DNA repair

Brain tumours and Gliomas, in particular, are among the primary causes of cancer mortality worldwide. Glioma diagnosis and therapy have not significantly improved despite decades of efforts. Autocrine TGF-β signalling promotes glioma proliferation, invasion, epithelial-to-mesenchymal transition (EMT), and drug resistance. Non-coding RNAs such as miRNA, lncRNA, and circRNAs have emerged as critical transcriptional and post-transcriptional regulators of TGF-β pathway components in glioma. Here, we summarize the complex regulatory network among regulatory ncRNAs and TGF-β pathway during Glioma pathogenesis and discuss their role as potential therapeutic targets for Gliomas.

Role of Non-Coding RNAs in TGF-β Signalling in Glioma

LINC01711 promotes transforming growth factor-beta (TGF-β) induced invasion in glioblastoma multiforme (GBM) by acting as a competing endogenous RNA for miR-34a and promoting ZEB1 expression

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