The m6A reader YTHDC1-mediated lncRNA CTBP1-AS2 m6A modification accelerates cholangiocarcinoma progression

Jin, Zhe; Liu, Yahui

doi:10.1016/j.heliyon.2023.e19816

Cited by 4 publications

(4 citation statements)

References 40 publications

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“…It was demonstrated that the CTBP1-AS2 overexpression reversed all AGE/LPS-induced effects including poor wound healing (Figure 4B), enhanced cell senescence (Figure 4C), and ROS production (Figure 4D). CTBP1-As2 has been shown to translocate into the cytoplasm to exert its influence on target molecules [36]. Here, we revealed that the level of CTBP1-AS2 expression was markedly upregulated in the cytoplasm of PDLFs after ErL irradiation (Figure 5A).…”

Section: The Stimulatory Effects Of Erl Irradiation On Ctbp1-as2 and ...mentioning

confidence: 75%

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Er:YAG Laser Alleviates Inflammaging in Diabetes-Associated Periodontitis via Activation CTBP1-AS2/miR-155/SIRT1 Axis

Ng,

Yu,

Chen

et al. 2024

IJMS

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Periodontitis is a significant health concern for individuals with diabetes mellitus (DM), characterized by inflammation and periodontium loss. Hyperglycaemia in DM exacerbates susceptibility to periodontitis by inducing inflammaging in the host immune system. The use of erbium-doped yttrium–aluminum–garnet laser (ErL) in periodontitis treatment has gained attention, but its impact on diabetic-associated periodontitis (DP) and underlying mechanisms remain unclear. In this study, we simulated DP by exposing human periodontal ligament fibroblasts (PDLFs) to advanced glycation end products (AGEs) and lipopolysaccharides from P. gingivalis (Pg-LPS). Subsequently, we evaluated the impact of ErL on the cells’ wound healing and assessed their inflammaging markers. ErL treatment promoted wound healing and suppressed inflammaging activities, including cell senescence, IL-6 secretion, and p65 phosphorylation. Moreover, the laser-targeted cells were observed to have upregulated expression of CTBP1-AS2, which, when overexpressed, enhanced wound healing ability and repressed inflammaging. Moreover, bioinformatic analysis revealed that CTBP1-AS2 acted as a sponge for miR155 and upregulated SIRT1. In conclusion, ErL demonstrated the ability to improve wound healing and mitigate inflammaging in diabetic periodontal tissue through the CTBP1-AS2/miR-155/SIRT1 axis. Targeting this axis could represent a promising therapeutic approach for preventing periodontitis in individuals with DM.

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Section: The Stimulatory Effects Of Erl Irradiation On Ctbp1-as2 and ...mentioning

confidence: 75%

“…CTBP1-As2 has been shown to translocate into the cytoplasm to exert its influence on target molecules [36]. Here, we revealed that the level of CTBP1-AS2 expression was markedly upregulated in the cytoplasm of PDLFs after ErL irradiation (Figure 5A).…”

Section: Mir-155 Is a Direct Target Of Ctbp1-as2 And Inhibition Of Mi...mentioning

confidence: 75%

Er:YAG Laser Alleviates Inflammaging in Diabetes-Associated Periodontitis via Activation CTBP1-AS2/miR-155/SIRT1 Axis

Ng,

Yu,

Chen

et al. 2024

IJMS

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“…YTHDC1 is the only YTH family methyl-binding protein located in the nucleus among m6A modifications (Xiao et al 2016 ), and it regulates a variety of metabolic responses by affecting the nuclear location, stability, attenuation, and splicing of RNAs, thereby influencing the development of diseases (Kasowitz et al 2018 ; Roundtree et al 2017 ; Widagdo et al 2022 ). YTHDC1 can interact with lncRNAs to perform different biological functions and regulate the occurrence and development of diseases (Jin and Liu 2023 ; Wu et al 2023 ). Tang et al found that LINC00857 interacted with YTHDC1 to regulate SLC7A5 and increase the stability of SLC7A5 mRNA, thus promoting the proliferation and migration of colorectal cancer cells (Tang et al 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Mir22hg facilitates ferritinophagy-mediated ferroptosis in sepsis by recruiting the m6A reader YTHDC1 and enhancing Angptl4 mRNA stability

Deng,

Zhong,

et al. 2024

J Bioenerg Biomembr

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Background Ferritinophagy-mediated ferroptosis plays a crucial role in fighting pathogen aggression. The long non-coding RNA Mir22hg is involved in the regulation of ferroptosis and aberrantly overexpression in lipopolysaccharide (LPS)-induced sepsis mice, but whether it regulates sepsis through ferritinophagy-mediated ferroptosis is unclear. Methods Mir22hg was screened by bioinformatics analysis. Ferroptosis was assessed by assaying malondialdehyde (MDA), reactive oxygen species (ROS), and Fe2+ levels, glutathione (GSH) activity, as well as ferroptosis-related proteins GPX4 and SLC3A2 by using matched kits and performing western blot. Ferritinophagy was assessed by Lyso tracker staining and FerroOrange staining, immunofluorescence analysis of Ferritin and LC-3, and western blot analysis of LC-3II/I, p62, FTH1, and NCOA4. The bind of YTH domain containing 1 (YTHDC1) to Mir22hg or angiopoietin-like-4 (Angptl4) was verified by RNA pull-down and/or immunoprecipitation (RIP) assays. Results Mir22hg silencing lightened ferroptosis and ferritinophagy in LPS-induced MLE-12 cells and sepsis mouse models, as presented by the downregulated MDA, ROS, Fe2+, NCOA4, and SLC3A2 levels, upregulated GPX4, GSH, and FTH1 levels, along with a decrease in autophagy. Mir22hg could bind to the m6A reader YTHDC1 without affecting its expression. Mechanistically, Mir22hg enhanced Angptl4 mRNA stability through recruiting the m6A reader YTHDC1. Furthermore, Angptl4 overexpression partly overturned Mir22hg inhibition-mediated effects on ferroptosis and ferritinophagy in LPS-induced MLE-12 cells. Conclusion Mir22hg contributed to in ferritinophagy-mediated ferroptosis in sepsis via recruiting the m6A reader YTHDC1 and strengthening Angptl4 mRNA stability, highlighting that Mir22hg may be a potential target for sepsis treatment based on ferroptosis.

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“…It is reported that YTHDF3 and YTHDF1 interactions with proteins associated with mRNA translation are blocked by O-GlcNAcylation, which inhibits the translation-promoting function [ 52 ]. Furthermore, YTHDC1-2 were another important m6A reader involved in RNA-related processes [ 53 , 54 ]. For example, YTHDC1 works as a splicing protein alternatively splicing its targets’ mRNA [ 55 ].…”

Section: Enzymes and Proteins Involved In Modification By M6amentioning

confidence: 99%

Recent advances of m6A methylation in skeletal system disease

Liang,

Yi,

Liu

et al. 2024

J Transl Med

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Skeletal system disease (SSD) is defined as a class of chronic disorders of skeletal system with poor prognosis and causes heavy economic burden. m6A, methylation at the N6 position of adenosine in RNA, is a reversible and dynamic modification in posttranscriptional mRNA. Evidences suggest that m6A modifications play a crucial role in regulating biological processes of all kinds of diseases, such as malignancy. Recently studies have revealed that as the most abundant epigentic modification, m6A is involved in the progression of SSD. However, the function of m6A modification in SSD is not fully illustrated. Therefore, make clear the relationship between m6A modification and SSD pathogenesis might provide novel sights for prevention and targeted treatment of SSD. This article will summarize the recent advances of m6A regulation in the biological processes of SSD, including osteoporosis, osteosarcoma, rheumatoid arthritis and osteoarthritis, and discuss the potential clinical value, research challenge and future prospect of m6A modification in SSD.

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The m6A reader YTHDC1-mediated lncRNA CTBP1-AS2 m6A modification accelerates cholangiocarcinoma progression

Cited by 4 publications

References 40 publications

Er:YAG Laser Alleviates Inflammaging in Diabetes-Associated Periodontitis via Activation CTBP1-AS2/miR-155/SIRT1 Axis

Er:YAG Laser Alleviates Inflammaging in Diabetes-Associated Periodontitis via Activation CTBP1-AS2/miR-155/SIRT1 Axis

Mir22hg facilitates ferritinophagy-mediated ferroptosis in sepsis by recruiting the m6A reader YTHDC1 and enhancing Angptl4 mRNA stability

Recent advances of m6A methylation in skeletal system disease

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