scholarly journals Comprehensive evaluation of differential long non‑coding RNA and gene expression in patients with cartilaginous endplate degeneration of cervical vertebra

2020 ◽  
Vol 20 (6) ◽  
pp. 1-1
Author(s):  
Jinghong Yuan ◽  
Jingyu Jia ◽  
Tianlong Wu ◽  
Xijuan Liu ◽  
Shen Hu ◽  
...  
Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 755
Author(s):  
Nur Atikah Zakaria ◽  
Md Asiful Islam ◽  
Wan Zaidah Abdullah ◽  
Rosnah Bahar ◽  
Abdul Aziz Mohamed Yusoff ◽  
...  

Thalassemia, an inherited quantitative globin disorder, consists of two types, α– and β–thalassemia. β–thalassemia is a heterogeneous disease that can be asymptomatic, mild, or even severe. Considerable research has focused on investigating its underlying etiology. These studies found that DNA hypomethylation in the β–globin gene cluster is significantly related to fetal hemoglobin (HbF) elevation. Histone modification reactivates γ-globin gene expression in adults and increases β–globin expression. Down-regulation of γ–globin suppressor genes, i.e., BCL11A, KLF1, HBG-XMN1, HBS1L-MYB, and SOX6, elevates the HbF level. β–thalassemia severity is predictable through FLT1, ARG2, NOS2A, and MAP3K5 gene expression. NOS2A and MAP3K5 may predict the β–thalassemia patient’s response to hydroxyurea, a HbF-inducing drug. The transcription factors NRF2 and BACH1 work with antioxidant enzymes, i.e., PRDX1, PRDX2, TRX1, and SOD1, to protect erythrocytes from oxidative damage, thus increasing their lifespan. A single β–thalassemia-causing mutation can result in different phenotypes, and these are predictable by IGSF4 and LARP2 methylation as well as long non-coding RNA expression levels. Finally, the coinheritance of β–thalassemia with α–thalassemia ameliorates the β–thalassemia clinical presentation. In conclusion, the management of β–thalassemia is currently limited to genetic and epigenetic approaches, and numerous factors should be further explored in the future.


Gene Reports ◽  
2021 ◽  
pp. 101257
Author(s):  
Eman Masoud Abd El Gayed ◽  
Ibrahim Fathi Zaid ◽  
Alaa Masoud Abd El Gayed ◽  
Aziza Mahmoud Mohamed Zaki ◽  
Eman Abd-allah Mahmoud Fouda

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e21523-e21523
Author(s):  
Lauren Sanders ◽  
Allison Cheney ◽  
Holly Beale ◽  
Ellen Kephart ◽  
Isabel Bjork ◽  
...  

e21523 Background: Diffuse pediatric gliomas harboring a Histone-H3 K27M mutation are more aggressive than H3-wild type gliomas and demonstrate global hypomethylation at the K27 residue1. As a result, these tumors show global aberrant gene expression, resulting in a stem-like proliferative cell population2. Posterior fossa (PF) ependymomas, on the other hand, harbor few significantly recurrent somatic mutations, but PF-A and PF-B subgroups have been defined on the basis of epigenetic differences3. Compared to PF-B, the PF-A subgroup demonstrates H3K27 hypomethylation, aberrant gene expression and aggressive tumor growth4,5. Methods: We recently identified a set of long non-coding RNA (lncRNA) that are transiently expressed in early brain development6, and hypothesized that H3K27M gliomas and PF-A ependymomas may share methylation-related dysregulation of lncRNA networks responsible for maintaining normal differentiation programs. Results: Here we describe a network of regulatory lncRNA with increased expression in both H3K27M gliomas and PF-A ependymomas, as compared to H3-WT gliomas and PF-B ependymomas. We demonstrate that increased expression of this lncRNA network correlates with the over-expression of signaling pathways involved in maintaining a non-differentiated, proliferative phenotype and driving tumorigenesis. Conclusions: We hypothesize that in both H3K27M gliomas and PF-A ependymomas, aberrant global methylation may be driving lncRNA to activate and maintain stem-like states in early neural development, suggesting similarities in epigenetically driven, developmental origins for both tumor types. References: 1. Chan KM, Fang D, Gan H, et al. Genes Dev. 2013;27(9):985-90; 2. Filbin MG, Tirosh I, Hovestadt V, et al. Science. 2018;360(6386):331-5; 3. Witt H, Mack SC, Ryzhova M, et al. Cancer cell. 2011;20(2):143-57; 4. Bayliss J, Mukherjee P, Lu C, et al. Sci. Transl. Med. 2016;8(366):366ra161; 5. Mack SC, Witt H, Piro RM, et al. Nature. 2014;506(7489):445; 6. Field AR, Jacobs FM, Fiddes IT, et al. bioRxiv. 2017:232553.


2018 ◽  
Vol 195 ◽  
pp. 318-319 ◽  
Author(s):  
Yansong Liu ◽  
Shuquan Rao ◽  
Yong Xu ◽  
Fuquan Zhang ◽  
Zhiqiang Wang ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Qingshui Wang ◽  
Youyu Lin ◽  
Wenting Zhong ◽  
Yu Jiang ◽  
Yao Lin

The death associated protein kinases (DAPKs) are a family of calcium dependent serine/threonine kinases initially identified in the regulation of apoptosis. Previous studies showed that DAPK family members, including DAPK1, DAPK2 and DAPK3 play a crucial regulatory role in malignant tumor development, in terms of cell apoptosis, proliferation, invasion and metastasis. Accumulating evidence has demonstrated that non-coding RNAs, including microRNA (miRNA), long non-coding RNA (lncRNA) and circRNA, are involved in the regulation of gene expression and tumorigenesis. Recent studies indicated that non-coding RNAs participate in the regulation of DAPKs. In this review, we summarized the current knowledge of non-coding RNAs, as well as the potential miRNAs, lncRNAs and circRNAs, that are involved in the regulation of DAPKs.


2020 ◽  
Author(s):  
Laura M. Saba ◽  
Paula L. Hoffman ◽  
Gregg E. Homanics ◽  
Spencer Mahaffey ◽  
Swapna Vidhur Daulatabad ◽  
...  

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