Long Non-Coding RNA (lncRNA) Roles in Cell Biology, Neurodevelopment and Neurological Disorders

Aliperti, Vincenza; Skonieczna, Justyna; Cerase, Andrea

doi:10.3390/ncrna7020036

Cited by 70 publications

(52 citation statements)

References 207 publications

(343 reference statements)

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“…Although there is currently less evidence than for miRNAs, altered brain expression of the RNA polymerase III-dependent ncRNA (i.e., NDM29, of the β-site amyloid precursor protein cleaving enzyme-1-antisense lncRNA (i.e., BACE1-AS), and of the intronic ncRNA (i.e., S1A) is known to be correlated to Aβ formation [ 287 , 288 , 289 ]. Moreover, increased cerebral tissue transcription of two lncRNAs, linc00507 and 17A, has been implicated in tau phosphorylation and GABA B alternative splicing, respectively [ 290 , 291 , 292 ]. Concerning possible circulating biomarkers, Feng et al report evidence for significant plasma lncRNA BACE1 upregulation in 88 AD patients when compared to 72 controls [ 257 ].…”

Section: Resultsmentioning

confidence: 99%

Blood-Based Biomarkers for Alzheimer’s Disease Diagnosis and Progression: An Overview

Varesi

Carrara

Pires

et al. 2022

Cells

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Alzheimer’s Disease (AD) is a progressive neurodegenerative disease characterized by amyloid-β (Aβ) plaque deposition and neurofibrillary tangle accumulation in the brain. Although several studies have been conducted to unravel the complex and interconnected pathophysiology of AD, clinical trial failure rates have been high, and no disease-modifying therapies are presently available. Fluid biomarker discovery for AD is a rapidly expanding field of research aimed at anticipating disease diagnosis and following disease progression over time. Currently, Aβ1–42, phosphorylated tau, and total tau levels in the cerebrospinal fluid are the best-studied fluid biomarkers for AD, but the need for novel, cheap, less-invasive, easily detectable, and more-accessible markers has recently led to the search for new blood-based molecules. However, despite considerable research activity, a comprehensive and up-to-date overview of the main blood-based biomarker candidates is still lacking. In this narrative review, we discuss the role of proteins, lipids, metabolites, oxidative-stress-related molecules, and cytokines as possible disease biomarkers. Furthermore, we highlight the potential of the emerging miRNAs and long non-coding RNAs (lncRNAs) as diagnostic tools, and we briefly present the role of vitamins and gut-microbiome-related molecules as novel candidates for AD detection and monitoring, thus offering new insights into the diagnosis and progression of this devastating disease.

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Section: Resultsmentioning

confidence: 99%

Blood-Based Biomarkers for Alzheimer’s Disease Diagnosis and Progression: An Overview

Varesi

Carrara

Pires

et al. 2022

Cells

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“…As PTCHD1-AS does not encode for a protein, its contribution to the etiology of ASD and ID is unclear. Emerging evidence suggests that lncRNAs govern the expression of coding genes by altering chromatin status, influencing the initiation of transcription, as well as by affecting mRNA stability post-transcriptionally [ 47 ]. To investigate this, Ross et al employed RNA fractionation and qRT-PCR to conclude that PTCHD1-AS was almost entirely localized to the nucleus, where it was also found to primarily associate with chromatin.…”

Section: Expression Profiling Of Ptchd1 and ...mentioning

confidence: 99%

PTCHD1: Identification and Neurodevelopmental Contributions of an Autism Spectrum Disorder and Intellectual Disability Susceptibility Gene

Pastore

Frankland

et al. 2022

Genes

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Over the last one and a half decades, copy number variation and whole-genome sequencing studies have illuminated the considerable genetic heterogeneity that underlies the etiologies of autism spectrum disorder (ASD) and intellectual disability (ID). These investigations support the idea that ASD may result from complex interactions between susceptibility-related genetic variants (single nucleotide variants or copy number variants) and the environment. This review outlines the identification and neurobiological characterization of two such genes located in Xp22.11, Patched domain-containing 1 (PTCHD1), and its antisense lncRNA PTCHD1-AS. Animal models of Ptchd1 disruption have recapitulated a subset of clinical symptoms related to ASD as well as to ID. Furthermore, these Ptchd1 mouse knockout studies implicate the expression of Ptchd1 in both the thalamic and the hippocampal brain regions as being crucial for proper neurodevelopment and cognitive function. Altered kynurenine metabolic signalling has been postulated as a disease mechanism in one of these animal studies. Additionally, ASD patient-derived induced pluripotent stem cells (iPSCs) carrying a copy number loss impacting the antisense non-coding RNA PTCHD1-AS have been used to generate 2D neuronal cultures. While copy number loss of PTCHD1-AS does not affect the transcription of PTCHD1, the neurons exhibit diminished miniature excitatory postsynaptic current frequency, supporting its role in ASD etiology. A more thorough understanding of risk factor genes, such as PTCHD1 and PTCHD1-AS, will help to clarify the intricate genetic and biological mechanisms that underlie ASD and ID, providing a foundation for meaningful therapeutic interventions to enhance the quality of life of individuals who experience these conditions.

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“…In recent years, studies have shown that long non-coding RNA (lncRNA) plays critical roles in breast cancer progression [ 3 , 4 ], which greatly supplements the gene regulation in this disease. LncRNAs execute their functions via various of paths such as transcription regulation, competitive endogenous RNA regulation and N6-Methyladenosine (m6A) modification [ 5 ]. In this study, the m6A regulation on lncRNA will be demonstrated.…”

Section: Introductionmentioning

confidence: 99%

MIR210HG promotes breast cancer progression by IGF2BP1 mediated m6A modification

et al. 2022

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Background Breast cancer is the most common cancer in women around the world, and the molecular mechanisms of breast cancer progression and metastasis are still unclear. This study aims to clarify the function and N6,2′-O-dimethyladenosine (m6A) regulation of lncRNA MIR210HG in breast cancer. Results High expression of MIR210HG was confirmed in breast cancer. MIR210HG promoted breast cancer progression, which was mediated by its encoded miR-210. MIR210HG was regulated by IGF2BP1 mediated m6A modification. IGF2BP1 was confirmed highly expressed in breast cancer and induced both MIR210HG and miR-210 expression, which contributed to breast cancer progression. In addition, MIR210HG transcript was stabilized by IGF2BP1 and co-factor ELAVL1. IGF2BP1 was a direct target of MYCN via E-box binding motif. MYCN induced IGF2BP1 expression in breast cancer cells. MIR210HG and miR-210 expressions were also increased by MYCN. Conclusions In breast cancer, MIR210HG functions as an oncogenic lncRNA, which is also mediated by its encoded miR-210. In addition, both IGF2BP1 and ELAVL1 enhance the stability of MIR210HG, which contributes to the progression of breast cancer. Interestingly, IGF2BP1 is directly activated by MYCN, which explains the oncogenic role of MYCN. These findings clarify the m6A regulation related molecular mechanism of breast cancer progression. The MYCN/IGF2BP1/MIR210HG axis may serve as an alternative molecular mechanism of breast cancer progression.

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Long Non-Coding RNA (lncRNA) Roles in Cell Biology, Neurodevelopment and Neurological Disorders

Cited by 70 publications

References 207 publications

Blood-Based Biomarkers for Alzheimer’s Disease Diagnosis and Progression: An Overview

Blood-Based Biomarkers for Alzheimer’s Disease Diagnosis and Progression: An Overview

PTCHD1: Identification and Neurodevelopmental Contributions of an Autism Spectrum Disorder and Intellectual Disability Susceptibility Gene

MIR210HG promotes breast cancer progression by IGF2BP1 mediated m6A modification

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