Long noncoding RNA and its contribution to autism spectrum disorders

Jing, Tang; Yu, Yizhen; Yang, Wei

doi:10.1111/cns.12710

Cited by 55 publications

(40 citation statements)

References 152 publications

(245 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, results from flow cytometry assay demonstrated that MEG3 over-expression enhanced the chemo-sensitivity of BC cells to DDP treatment ( Figure 3C). Moreover, results of western blot analysis revealed that DDP treatment further up-regulated the protein levels of cleaved caspase-3 and LncRNAs has been extensively researched in a variety of pathophysiological processes, including autism spectrum disorders [21], cancers [22], cardiovascular disease [23], Alzheimer's disease [24] and in reproduction and development [25]. Because prior findings revealed low expression of MEG3 in BC tissues [19], we conducted in vitro experiments using T24 and 5637 cells to investigate the role of MEG3 in the metastasis and chemotherapy sensitivity of BC cells.…”

Section: Effects Of Meg3 Over-expression On Bc Cell Migration and Invmentioning

confidence: 99%

Up-regulation of LncRNA MEG3 inhibits cell migration and invasion and enhances cisplatin chemosensitivity in bladder cancer cells

Feng

Zhang

Fan

et al. 2018

neo

View full text Add to dashboard Cite

It has been proven that maternally expressed 3 (MEG3), a long non-coding RNA (LncRNA), is down-regulated and inversely correlated with prognosis in various types of cancer, including bladder cancer (BC). Nevertheless, the role of MEG3 in BC has not been fully identified. Herein, we found that MEG3 expression was reduced in 21 BC tumor tissue samples compared to corresponding adjacent tissues. We then established T24 and 5637 cells with a stably integrated expression of MEG3 by G418 resistance screening, and data revealed that the BC cells over-expressing MEG3 displayed weaker migration and invasion ability than control cells. The expression and activity of matrix metalloproteinase (MMP)2 and MMP9 were down-regulated when MEG3 was over-expressed. Moreover, MEG3 over-expression sensitized BC cells to the chemotherapy drug cisplatin (DDP). DDP treatment significantly induced cell apoptosis, down-regulated bcl2 expression, and up-regulated cleaved-caspase-3 and bax expression in BC cells with MEG3 over-expression. MEG3 and p53 can also stimulate mutual expression in BC cells, thus indicating a potential positive feedback loop of MEG3 and p53. Our combined results suggest that over-expression of MEG3 inhibits migration and invasion and enhances DDP chemo-sensitivity in bladder cancer cells.

show abstract

Section: Effects Of Meg3 Over-expression On Bc Cell Migration and Invmentioning

confidence: 99%

Up-regulation of LncRNA MEG3 inhibits cell migration and invasion and enhances cisplatin chemosensitivity in bladder cancer cells

Feng

Zhang

Fan

et al. 2018

neo

View full text Add to dashboard Cite

show abstract

“…An increasing number of studies have found that lncRNAs regulate development of the central nervous system through multiple pathways . Recent studies have revealed that lncRNAs may regulate the pathogenesis of ASD at the epigenetic level . A total of 3929 differentially expressed lncRNAs have been identified in ASD patients, of which 2407 are upregulated and 1522 are downregulated, suggesting that lncRNAs may play regulatory roles in ASD .…”

Section: Introductionmentioning

confidence: 99%

Effect of the autism‐associated lncRNA Shank2‐AS on architecture and growth of neurons

Luo

Liu

Wang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

The pathogenic mechanism of autism is complex, and current research has shown that long noncoding RNAs (lncRNAs) may play important roles in this process. The antisense lncRNA of SH3 and multiple ankyrin repeat domains 2 (Shank2-AS) is upregulated in patients with autism spectrum disorder (ASD), whereas the expression of its sense strand gene Shank2 is downregulated. In neuronal cells, Shank2-AS and Shank2 can form a double-stranded RNA and inhibit Shank2 expression. Overexpression of Shank2-AS decreases neurite numbers and lengths, thereby inhibiting the proliferation of neuronal cells and promoting their apoptosis. Overexpression of Shank2 inhibits the abovementioned effects of Shank2-AS, and transfection of a vector containing the 10th intron of Shank2 (Shank2-AS is reverse-transcribed from this region) also blocks the function of Shank2-AS. Shank2 small interfering RNA plays a role similar to Shank2-AS. Therefore, Shank2-AS is abnormally expressed in patients with ASD and may affect the structure and growth of neurons by regulating Shank2 expression, thereby facilitating the development of ASD.

show abstract

“…The abnormally expanded CGG segment results in silencing of the FMR1 gene with subsequent abnormalities in the formation and function of synapses [ 141 ]. Intriguingly, several lncRNAs, including FMR4 , FMR5 , FMR6 and FMR1-AS , are transcribed from the FMR1 gene locus as well [ 142 ]. Using gene expression microarrays, Peschansky et al identified a wide array of FMR4 -responsive genes, suggesting a broad role of FMR4 [ 143 ].…”

Section: Lncrnas In Human Diseasesmentioning

confidence: 99%

Molecular mechanisms of long noncoding RNAs and their role in disease pathogenesis

et al. 2018

View full text Add to dashboard Cite

LncRNAs are long non-coding regulatory RNAs that are longer than 200 nucleotides. One of the major functions of lncRNAs is the regulation of specific gene expression at multiple steps including, recruitment and expression of basal transcription machinery, post-transcriptional modifications and epigenetics [1]. Emerging evidence suggests that lncRNAs also play a critical role in maintaining tissue homeostasis during physiological and pathological conditions, lipid homeostasis, as well as epithelial and smooth muscle cell homeostasis, a topic that has been elegantly reviewed [2–5]. While aberrant expression of lncRNAs has been implicated in several disease conditions, there is paucity of information about their contribution to the etiology of diseases [6]. Several studies have compared the expression of lncRNAs under normal and cancerous conditions and found differential expression of several lncRNAs, suggesting thereby an involvement of lncRNAs in disease processes [7, 8]. Furthermore, the ability of lncRNAs to influence epigenetic changes also underlies their role in disease pathogenesis since epigenetic regulation is known to play a critical role in many human diseases [1]. LncRNAs thus are not only involved in homeostatic functioning but also play a vital role in the progression of many diseases, thereby underscoring their potential as novel therapeutic targets for the alleviation of a variety of human disease conditions.

show abstract

Long noncoding RNA and its contribution to autism spectrum disorders

Cited by 55 publications

References 152 publications

Up-regulation of LncRNA MEG3 inhibits cell migration and invasion and enhances cisplatin chemosensitivity in bladder cancer cells

Up-regulation of LncRNA MEG3 inhibits cell migration and invasion and enhances cisplatin chemosensitivity in bladder cancer cells

Effect of the autism‐associated lncRNA Shank2‐AS on architecture and growth of neurons

Molecular mechanisms of long noncoding RNAs and their role in disease pathogenesis

Contact Info

Product

Resources

About