RNA editing is induced by type I interferon in esophageal squamous cell carcinoma

Zhang, Jinyao; Chen, Zhaoli; Tang, Zefang; Huang, Jianbing; Hu, Xueda; He, Jie

doi:10.1177/1010428317708546

Cited by 11 publications

(8 citation statements)

References 40 publications

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“…A venn diagram was constructed to intersect the two sets of results, identifying a total of 97 genes associated with OS. A number of genes were found to have prognostic value for patients with ESCC, including FOS (24), Adenosine Deaminase RNA Specific (25,26), Karyopherin Subunit α 2 (27) and Translocator protein (28). These genes were enriched in a number of signaling pathways, including DNA replication, protein processing in endoplasmic reticulum and influenza, as demonstrated using KEGG analysis.…”

Section: Discussionmentioning

confidence: 99%

A five‑gene signature to predict the overall survival time of patients with esophageal squamous cell carcinoma

Yan

et al. 2019

Oncol Lett

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Esophageal squamous cell carcinoma (ESCC) is one of the six most commonly diagnosed tumor types in the Chinese population. Gene expression profiles help to predict the prognosis of patients with ESCC. Disease recurrence as the survival endpoint has been analyzed in the majority of previous studies; therefore, the aim of the present study was to construct a robust gene signature in order to determine the overall survival (OS) of patients with ESCC. The gene expression and clinical data of patients with ESCC were downloaded from The Cancer Genome Atlas (TCGA) database. Of the selected data (172 samples from surviving patients), 72 samples were randomly selected as modeling data, and verification was conducted using the entire dataset. Data from the Gene Expression Omnibus was analyzed simultaneously, and a venn diagram was constructed to determine the intersection between these two sets of results; a total of 97 genes were found to be associated with OS. Kyoto Encyclopedia of Genes and Genomes analysis demonstrated that these genes were primarily associated with specific pathways (Homo sapiens), including DNA replication, protein processing in endoplasmic reticulum and influenza A. A five-gene signature was identified with a robust likelihood-based survival modeling approach. Using regression coefficient modeling, a prognostic model consisting of the C-X-C motif chemokine ligand 8, DNA damage inducible transcript 3, RAB27A, member RAS oncogene family, replication factor C subunit 2 and elongation factor for RNA polymerase II 2 genes was constructed and validated. Based on these results, patients were subdivided into high and low-risk groups. Compared with the high-risk group, the OS time of patients in the low-risk group was significantly increased. Furthermore, it was determined that the five genes were all differentially expressed in ESCC tissues compared with normal tissues, indicating the potential role of these genes in ESCC initiation and progression. In another independent cohort, this five-gene signature was further confirmed and was considered as an independent prognostic biomarker for OS prediction in patients with ESCC. In conclusion, the OS of patients with ESCC may be predicted using this five-gene signature, which may be useful in identifying patients with high-risk ESCC.

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Section: Discussionmentioning

confidence: 99%

A five‑gene signature to predict the overall survival time of patients with esophageal squamous cell carcinoma

Yan

et al. 2019

Oncol Lett

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“…High expression of ADAR1 in cancers may be caused by ADAR gene amplification, and interferon response due to chronic inflammation (Fumagalli et al, 2015). Furthermore, JAK–STAT signaling pathway activation has been associated with increased ADAR1 levels in malignancies (Zhang et al, 2017; Zipeto et al, 2016). A previous study revealed that the increased JAK2 signaling and breakpoint cluster region‐Abelson murine leukemia 1 amplification activate ADAR1 expression in blast crisis chronic myeloid leukemia progenitors (Zipeto et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

RNA editing enzyme adenosine deaminases acting on RNA 1 deficiency increases the sensitivity of non‐small cell lung cancer cells to anlotinib by regulating CX3CR1‐fractalkine expression

Jin

Cao

et al. 2021

Drug Development Research

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Adenosine deaminases acting on RNA 1 (ADAR1) has been identified to play key roles in non‐small cell lung cancer (NSCLC) progression, and can modulate the sensitivity of cancer cells to anticancer drugs. The current study aimed to investigate the effect of ADAR1 on the sensitivity of NSCLC cells to anlotinib. We established anlotinib‐resistant NSCLC (NSCLC/AR) cells, including NCI‐H1975/AR and A549/AR cells. Results showed that ADAR1 was significantly upregulated in NSCLC/AR cells. Genetic‐knockdown of ADAR1 increased the sensitivity of NSCLC/AR cells to anlotinib by inducing cell proliferation suppression, cell cycle arrest, and apoptosis. Furthermore, knockdown of ADAR1 decreased the level of C‐X3‐C motif chemokine ligand 1 (CX3CL1) in NCI‐H1975/AR and A549/AR cells after anlotinib treatment. Introduction of exogenous CX3CL1 significantly reversed the positive effect of ADAR1 deficiency on NSCLC/AR cell sensitivity, exhibited by the increase of cell viability and decrease of apoptosis. Further in‐vivo study demonstrated that knockdown of ADAR1 inhibited NCI‐H1975/AR cell tumorigenesis by reducing CX3CL1 expression. Collectively, ADAR1 deficiency increased the sensitivity of NSCLC/AR cells to anlotinib by downregulating CX3CL1, which might provide a potential strategy for NSCLC/AR therapy.

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“…AZIN1 ‐dependent editing, together with FLNB A‐to‐I edition, is also involved in the pathogenesis of ESCC (Qin et al, 2014). Interestingly, type I IFNs and their associated JAK/STAT pathways, up‐regulate ADAR1 expression resulting in aberrant A‐to‐I editing process in ESCC (Zhang, Chen, Tang, et al, 2017). In contrast, a tumour suppressor role for ADAR2 has been described and down‐regulation of ADAR2 enzyme has been linked to ESCC progression.…”

Section: De‐regulated Epitranscriptome In Cancermentioning

confidence: 99%

Towards a druggable epitranscriptome: Compounds that target RNA modifications in cancer

Esteller

2021

British J Pharmacology

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Epitranscriptomics is an exciting emerging area that studies biochemical modifications of RNA. The field is boosted by the technical efforts of the last decade to characterize and quantify RNA modifications which have led to a map of post-transcripcional RNA marks in normal cell fate and develoment. However, the scientific interest has been fueled by the discovery of aberrant epitranscriptomes associated with human diseases, mainly cancer. The challenge is now to see whether epitrancriptomics offers a tunable mechanims to be targeted by small-molecule intervention. In this review, we will describe the principal RNA modifications (with a focus on mRNA), summarize the latest scientific evidences of their dysregulation in cancer and provide an overview of the state-of-the-art drug discovery to target the epitranscriptome. Finally, we will discuss the principal challenges in the field of chemical biology and drug development to increase the potential of targeted-RNA for clinical benefit.

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RNA editing is induced by type I interferon in esophageal squamous cell carcinoma

Cited by 11 publications

References 40 publications

A five‑gene signature to predict the overall survival time of patients with esophageal squamous cell carcinoma

A five‑gene signature to predict the overall survival time of patients with esophageal squamous cell carcinoma

RNA editing enzyme adenosine deaminases acting on RNA 1 deficiency increases the sensitivity of non‐small cell lung cancer cells to anlotinib by regulating CX3CR1‐fractalkine expression

Towards a druggable epitranscriptome: Compounds that target RNA modifications in cancer

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