Breaking paradigms: Long non-coding RNAs forming gene fusions with potential implications in cancer

Sánchez-Marín, David; Silva-Cázares, Macrina Beatriz; Porras-Reyes, Fany Iris; García-Román, Rebeca; Campos-Parra, Alma D.

doi:10.1016/j.gendis.2023.101136

Cited by 4 publications

(3 citation statements)

References 108 publications

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“…It has recently become evident that lncRNA genes are commonly subject to fusion with genes encoding other RNAs, including mRNAs and lncRNAs. In breast cancer, there has been documentation of several fusions involving the PVT1 lncRNA (plasmacytoma variant translocation 1), which resides in a fragile site on chromosome 8 and is implicated in a variety of cancers [ 39 ]. Amplification of PVT1 has been found to stabilize oncoproteins, including STAT3 and KLF5 [ 40 , 41 ].…”

Section: Genomic Alterations Affecting Cernas and Cernets In Tnbcmentioning

confidence: 99%

“…The lncRNA PVT1 promotes TNBC tumorigenesis through KLF5/β-catenin signaling [ 40 ]. As discussed above, several regulatory PVT1 fusions have been identified in breast cancer [ 39 ]. CircTADA2A, which is downregulated in TNBC tissues, promotes SOCS3 expression, metastasis and an aggressive oncogenic phenotype through competition with miR-203a [ 63 ].…”

Section: Significance Of Cernets Alterations In Tnbcmentioning

confidence: 99%

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Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC)

Qattan

2024

IJMS

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The concept of competitive endogenous RNA regulation has brought on a change in the way we think about transcriptional regulation by miRNA–mRNA interactions. Rather than the relatively simple idea of miRNAs negatively regulating mRNA transcripts, mRNAs and other non-coding RNAs can regulate miRNAs and, therefore, broad networks of gene products through competitive interactions. While this concept is not new, its significant roles in and implications on cancer have just recently come to light. The field is now ripe for the extrapolation of technologies with a substantial clinical impact on cancer. With the majority of the genome consisting of non-coding regions encoding regulatory RNAs, genomic alterations in cancer have considerable effects on these networks that have been previously unappreciated. Triple-negative breast cancer (TNBC) is characterized by high mutational burden, genomic instability and heterogeneity, making this aggressive breast cancer subtype particularly relevant to these changes. In the past few years, much has been learned about the roles of competitive endogenous RNA network regulation in tumorigenesis, disease progression and drug response in triple-negative breast cancer. In this review, we present a comprehensive view of the new knowledge and future perspectives on competitive endogenous RNA networks affected by genomic alterations in triple-negative breast cancer. An overview of the competitive endogenous RNA (ceRNA) hypothesis and its bearing on cellular function and disease is provided, followed by a thorough review of the literature surrounding key competitive endogenous RNAs in triple-negative breast cancer, the genomic alterations affecting them, key disease-relevant molecular and functional pathways regulated by them and the clinical implications and significance of their dysregulation. New knowledge of the roles of these regulatory mechanisms and the current acceleration of research in the field promises to generate insights into the diagnosis, classification and treatment of triple-negative breast cancer through the elucidation of new molecular mechanisms, therapeutic targets and biomarkers.

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Section: Genomic Alterations Affecting Cernas and Cernets In Tnbcmentioning

confidence: 99%

Section: Significance Of Cernets Alterations In Tnbcmentioning

confidence: 99%

Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC)

Qattan

2024

IJMS

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“…Numerous fusion events involving lncRNAs have been reported, with their outcomes largely dependent on the specific positions of the lncRNA partners. While lncRNA-mRNA and lncRNA-lncRNA fusions are likely to remain as transcripts, mRNA-lncRNA fusions can result in the production of proteins with oncogenic functions ( 97 ). A pan-cancer bioinformatic study by Guo et al.…”

Section: Types Of Fusion Gene Partnersmentioning

confidence: 99%

Cancer fusion transcripts with human non-coding RNAs

Mohammad,

Zolotovskaia,

Suntsova

et al. 2024

Front. Oncol.

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Cancer chimeric, or fusion, transcripts are thought to most frequently appear due to chromosomal aberrations that combine moieties of unrelated normal genes. When being expressed, this results in chimeric RNAs having upstream and downstream parts relatively to the breakpoint position for the 5’- and 3’-fusion components, respectively. As many other types of cancer mutations, fusion genes can be of either driver or passenger type. The driver fusions may have pivotal roles in malignisation by regulating survival, growth, and proliferation of tumor cells, whereas the passenger fusions most likely have no specific function in cancer. The majority of research on fusion gene formation events is concentrated on identifying fusion proteins through chimeric transcripts. However, contemporary studies evidence that fusion events involving non-coding RNA (ncRNA) genes may also have strong oncogenic potential. In this review we highlight most frequent classes of ncRNAs fusions and summarize current understanding of their functional roles. In many cases, cancer ncRNA fusion can result in altered concentration of the non-coding RNA itself, or it can promote protein expression from the protein-coding fusion moiety. Differential splicing, in turn, can enrich the repertoire of cancer chimeric transcripts, e.g. as observed for the fusions of circular RNAs and long non-coding RNAs. These and other ncRNA fusions are being increasingly recognized as cancer biomarkers and even potential therapeutic targets. Finally, we discuss the use of ncRNA fusion genes in the context of cancer detection and therapy.

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Architects and Partners: The Dual Roles of Non-coding RNAs in Gene Fusion Events

Dorney,

Reis-das-Mercês,

Schmitz

2024

Methods in Molecular Biology

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Breaking paradigms: Long non-coding RNAs forming gene fusions with potential implications in cancer

Cited by 4 publications

References 108 publications

Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC)

Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC)

Cancer fusion transcripts with human non-coding RNAs

Architects and Partners: The Dual Roles of Non-coding RNAs in Gene Fusion Events

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