Figure - available from: Journal of Clinical Laboratory Analysis
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Conjoint analysis of MeRIP‐seq and RNA‐seq data. (A) Volcano plots expressed the numbers of lncRNAs with significantly differential m6A peaks. (B) Volcano plots showed the differential expressed lncRNAs. (C) The four‐quadrant diagram showed the m6A methylation lncRNAs and differentially expressed lncRNAs. The red dots expressed downregulated lncRNAs with hypermethylation, the blue dots expressed downregulated lncRNAs with hypomethylation, and the green dots expressed upregulated lncRNAs with hypomethylation. (D) Peak of lncRNAs in the METTL14‐overexpression and control group
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Background
Emerging studies have demonstrated the critical role of RNA m6A methylation in tumor progression, whereas lncRNA m6A modification profiles in breast cancer remain largely unknown. Our previous study has shown that METTL14 accelerates breast cancer migration and invasion in an m6A‐dependent manner, making it critical to analyze METTL14‐me...
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Citations
... Furthermore, METTL14-mediated m6A modification improves the m6A level of the oncogenic molecule lncRNA AC084125.2 in MDA-MB-231 cells and down-regulates its expression, facilitating BC cell migration and invasion. However, the precise mechanism behind this effect requires further investigation.72 In both MDA-MB-231 and MCF-7 cells, KIAA1429 targets the m6A modification site of LINC00667 to enhance its mRNA stability. ...
In recent years, breast cancer (BC) has surpassed lung cancer as the most common malignant tumor worldwide and remains the leading cause of cancer death in women. The etiology of BC usually involves dysregulation of epigenetic mechanisms and aberrant expression of certain non‐coding RNAs (ncRNAs). N6‐methyladenosine (m6A), the most prevalent RNA modification in eukaryotes, widely exists in ncRNAs to affect its biosynthesis and function, and is an important regulator of tumor‐related signaling pathways. Interestingly, ncRNAs can also regulate or target m6A modification, playing a key role in cancer progression. However, the m6A‐ncRNAs regulatory network in BC has not been fully elucidated, especially the regulation of m6A modification by ncRNAs. Therefore, in this review, we comprehensively summarize the interaction mechanisms and biological significance of m6A modifications and ncRNAs in BC. Meanwhile, we also focused on the clinical application value of m6A modification in BC diagnosis and prognosis, intending to explore new biomarkers and potential therapeutic targets.
... Additionally, NORAD-silenced cells present reduced invasion, migration, cell viability and colony formation [34], and xenograft BC mouse models established with NORAD-silenced cells present development of smaller tumors [35]. NORAD is also significantly upregulated in BC-derived exosomes, associated with increased m6A methylation [36,37]. In other studies, NORAD is considered a tumor suppressor as its expression levels are lower in BC tissues and cancer cells compared to normal conditions, leading to increased cell proliferation, migration and invasion, LNM development and poor prognosis [38,39]. ...
Simple Summary
Breast cancer (BC) is a heterogeneous disease classified into different subtypes presenting several treatment challenges, especially in more advanced cases arising from triple negative breast cancer. NORAD is a long non-coding RNA (lncRNA) activated by DNA damage, with an impacting role in the repair process of DNA insults. This lncRNA is differentially expressed in BC subtypes, participating in cancer initiation and progression, by interacting with an extended range of signaling partners. Here, we review the network of NORAD molecular interactions with relevance, as well as NORAD’s potential as a prognostic, predictive and target for BC treatment.
Abstract
Long non-coding RNA activated by DNA damage (NORAD) has recently been associated with pathologic mechanisms underlying cancer progression. Due to NORAD’s extended range of interacting partners, there has been contradictory data on its oncogenic or tumor suppressor roles in BC. This review will summarize the function of NORAD in different BC subtypes and how NORAD impacts crucial signaling pathways in this pathology. Through the preferential binding to pumilio (PUM) proteins PUM1 and PUM2, NORAD has been shown to be involved in the control of cell cycle, angiogenesis, mitosis, DNA replication and transcription and protein translation. More recently, NORAD has been associated with PUM-independent roles, accomplished by interacting with other ncRNAs, mRNAs and proteins. The intricate network of NORAD-mediated signaling pathways may provide insights into the potential design of novel unexplored strategies to overcome chemotherapy resistance in BC treatment.
The N6‐methyladenosine (m6A) RNA modification has gained significant prominence as a new layer of regulatory mechanism that governs gene expression. Over the past decade, various m6A regulators responsible for introducing, eliminating, and recognising RNA methylation have been identified. Notably, these m6A regulators often exhibit altered expression patterns in cancer, occasionally offering prognostic value. Nonetheless, the complex roles of these regulators in human cancer pathology remain enigmatic, with conflicting outcomes reported in different studies.In recent years, a multitude of inhibitors and activators targeting m6A regulators have been reported. Several of these compounds have demonstrated promising efficacy in both in vitro and in vivo cancer models. These findings collectively underscore the dynamic landscape of m6A regulation in cancer biology, revealing its potential as a therapeutic target and prognostic indicator.
