LINC00261 Inhibits Esophageal Cancer Radioresistance by Down-Regulating microRNA-552-3p and Promoting DIRAS1

Yang, Baolong; Ma, Hongbing; Bian, Yan

doi:10.2147/cmar.s332640

Cited by 2 publications

(2 citation statements)

References 34 publications

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“…Supplementary Table S2 listed the lncRNAs involved in cancer radioresistance/radiosensitivity and their concise mechanisms. The sources of cancer included bladder cancer ( Tan et al, 2015 ; Jiang et al, 2017 ), breast cancer ( Liu et al, 2019a ; Zhang et al, 2019a ; Wang et al, 2019 ; Qian et al, 2020 ; Zhang et al, 2020a ), cardiac cancer ( Jia et al, 2019 ), gastric cancer ( Jiang et al, 2020 ; Lu et al, 2020 ; Xiao et al, 2020 ), cervical cancer ( Jing et al, 2015 ; Li et al, 2018a ; Han et al, 2018 ; Gao et al, 2019 ; Zhao et al, 2019 ; Wang et al, 2020a ; Ge et al, 2020 ), colorectal cancer ( Liu et al, 2020a ; Liu et al, 2020b ; Li et al, 2021 ; Liang et al, 2021 ), esophageal cancer ( Li et al, 2017 ; Chen et al, 2018a ; Zhang et al, 2019b ; Wang et al, 2020b ; Cheng et al, 2020 ; Liu et al, 2021a ; Sun et al, 2021 ; Yang et al, 2021 ), glioblastoma ( Li et al, 2018b ; Ahmadov et al, 2021 ; Li et al, 2022 ), glioma ( Yang et al, 2016 ; Zheng et al, 2016 ; Wang et al, 2020c ; Wang et al, 2020d ; Tang et al, 2020 ; Zheng et al, 2020 ; Gao et al, 2021 ; Tian et al, 2021 ), head and neck squamous cell cancer ( Li et al, 2020a ), laryngeal cancer ( Cui et al, 2019 ; Tang et al, 2019 ; Tang and Shan, 2019 ), nasopharyngeal cancer ( Jin et al, 2016 ; Wang et al, 2017 ; Ma et al, 2018 ; Yi et al, 2019 ; Han et al, 2020a ; Han et al, 2020b ; Wang et al, 2020e ; ...…”

Section: Resultsmentioning

confidence: 99%

The Mechanism of Long Non-coding RNA in Cancer Radioresistance/Radiosensitivity: A Systematic Review

Zhang

2022

Front. Pharmacol.

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Background and purpose: Radioresistance remains a significant challenge in tumor therapy. This systematic review aims to demonstrate the role of long non-coding RNA (lncRNA) in cancer radioresistance/radiosensitivity.Material and methods: The electronic databases Pubmed, Embase, and Google Scholar were searched from January 2000 to December 2021 to identify studies addressing the mechanisms of lncRNAs in tumor radioresistance/sensitivity, each of which required both in vivo and in vitro experiments.Results: Among the 87 studies identified, lncRNAs were implicated in tumor radioresistance/sensitivity mainly in three paradigms. 1) lncRNAs act on microRNA (miRNA) by means of a sponge, and their downstream signals include some specific molecular biological processes (DNA repair and chromosome stabilization, mRNA or protein stabilization, cell cycle and proliferation, apoptosis-related pathways, autophagy-related pathways, epithelial-mesenchymal transition (EMT), cellular energy metabolism) and some signaling mediators (transcription factors, kinases, some important signal transduction pathways) that regulate various biological processes. 2) lncRNAs directly interact with proteins, affecting the cell cycle and autophagy to contribute to tumor radioresistance. 3) lncRNAs act like transcription factors to initiate downstream signaling pathways and participate in tumor radioresistance.Conclusion: lncRNAs are important regulators involved in tumor radioresistance\sensitivity. Different lncRNAs may participate in the radioresistance with the same regulatory paradigm, and the same lncRNAs may also participate in the radioresistance in different ways. Future research should focus more on comprehensively characterizing the mechanisms of lncRNAs in tumor radioresistance to help us identify corresponding novel biomarkers and develop new lncRNA-based methods to improve radioresistance.

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Section: Resultsmentioning

confidence: 99%

The Mechanism of Long Non-coding RNA in Cancer Radioresistance/Radiosensitivity: A Systematic Review

Zhang

2022

Front. Pharmacol.

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“…For the long non‐coding RNA LINC00261 is known, that the gene product is a negative regulator of cell growth and therefore might play a role in the promotion of differentiation and apoptosis (Yang, Ma, & Bian, 2021), but there is no published data with regards to ADHD or other mental disorders yet. The increased expression of LINC00261 in the PARK2 ADHD duplication carrier might hint at a role in the delayed brain maturation that is suggested in ADHD pathogenesis (Shaw et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

ADHD‐associated PARK2 copy number variants: A pilot study on gene expression and effects of supplementary deprivation in patient‐derived cell lines

Radtke

Palladino

McNeill

et al. 2022

American J of Med Genetics Pt B

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Recent studies show an association of Parkin RBR E3 ubiquitin protein ligase (PARK2) copy number variations (CNVs) with attention deficit hyperactivity disorder (ADHD). The aim of our pilot study to investigate gene expression associated with PARK2 CNVs in human‐derived cellular models. We investigated gene expression in fibroblasts, hiPSC and dopaminergic neurons (DNs) of ADHD PARK2 deletion and duplication carriers by qRT PCR compared with healthy and ADHD cell lines without PARK2 CNVs. The selected 10 genes of interest were associated with oxidative stress response (TP53, NQO1, and NFE2L2), ubiquitin pathway (UBE3A, UBB, UBC, and ATXN3) and with a function in mitochondrial quality control (PINK1, MFN2, and ATG5). Additionally, an exploratory RNA bulk sequencing analysis in DNs was conducted. Nutrient deprivation as a supplementary deprivation stress paradigm was used to enhance potential genotype effects. At baseline, in fibroblasts, hiPSC, and DNs, there was no significant difference in gene expression after correction for multiple testing. After nutrient deprivation in fibroblasts NAD(P)H‐quinone‐dehydrogenase 1 (NQO1) expression was significantly increased in PARK2 CNV carriers. In a multivariate analysis, ubiquitin C (UBC) was significantly upregulated in fibroblasts of PARK2 CNV carriers. RNA sequencing analysis of DNs showed the strongest significant differential regulation in Neurontin (NNAT) at baseline and after nutrient deprivation. Our preliminary results suggest differential gene expression in pathways associated with oxidative stress, ubiquitine‐proteasome, immunity, inflammation, cell growth, and differentiation, excitation/inhibition modulation, and energy metabolism in PARK2 CNV carriers compared to wildtype healthy controls and ADHD patients.

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LINC00261 Inhibits Esophageal Cancer Radioresistance by Down-Regulating microRNA-552-3p and Promoting DIRAS1

Cited by 2 publications

References 34 publications

The Mechanism of Long Non-coding RNA in Cancer Radioresistance/Radiosensitivity: A Systematic Review

The Mechanism of Long Non-coding RNA in Cancer Radioresistance/Radiosensitivity: A Systematic Review

ADHD‐associated PARK2 copy number variants: A pilot study on gene expression and effects of supplementary deprivation in patient‐derived cell lines

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