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Cancers
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RNA in Non-Small-Cell Lung Cancer
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RNA in Non-Small-Cell Lung Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 3165

Special Issue Editor

Dr. Silvia Catuogno

E-Mail Website
Guest Editor
Institute Experimental Endocrinology and Oncology “Gaetano Salvatore” (IEOS), National Research Council (CNR), 80131 Naples, Italy
Interests: aptamers; cancer; target therapy; targeted delivery strategies; non-coding RNAs

Special Issue Information

Dear Colleagues, 

Non-small-cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. Patients often face resistance to common therapies, showing a poor prognosis. In fact, despite recent advances, most patients are diagnosed at advanced stages, with a very low overall survival. Therefore, the identification of new effective diagnostic and therapeutic strategies for NSCLC patients is a crucial challenge in oncology.

In this context, non-coding RNAs (ncRNAs), key regulators of gene expression at transcriptional and post-transcriptional levels, represent a promising class of molecules. Through cancer cell profiling, miRNAs and lnc-RNAs, which importantly contribute to NSCLC molecular characterization, can be identified and used for effective diagnosis. Moreover, based on their role, miRNAs and lnc-RNAs can also enable the design of innovative NSCLC therapeutics. In addition to endogenous ncRNAs, such as miRNAs and lnc-RNAs, exogenous ncRNAs, including Antisense Oligonucleotides (ASOs), short interfering RNAs (siRNAs) and RNA aptamers, are very promising for NSCLC diagnosis and/or target therapy.

This Special Issue will report recent advancements in the field of ncRNAs in NSCLC, covering key aspects of their applications in diagnosis and target therapy.

Dr. Silvia Catuogno
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • NSCLC
  • non-coding RNAs
  • miRNAs
  • lnc-RNAs
  • ASOs
  • siRNAs
  • aptamers
  • diagnosis
  • target therapy

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Published Papers (3 papers)

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Research

15 pages, 2466 KiB  
Article
Profiling Plasma Extracellular Vesicle Metabotypes and miRNAs: An Unobserved Clue for Predicting Relapse in Patients with Early-Stage NSCLC
by Vivi Bafiti, Eleni Thanou, Sotiris Ouzounis, Athanasios Kotsakis, Vasilis Georgoulias, Evi Lianidou, Theodora Katsila and Athina Markou
Cancers 2024, 16(22), 3729; https://doi.org/10.3390/cancers16223729 - 5 Nov 2024
Viewed by 504
Abstract
Background and Objective: Lung cancer, the second most prevalent cancer globally, poses significant challenges in early detection and prognostic assessment. Despite advancements in targeted therapies and immunotherapy, the timely identification of relapse remains elusive. Blood-based liquid biopsy biomarkers, including circulating tumor cells (CTCs), [...] Read more.
Background and Objective: Lung cancer, the second most prevalent cancer globally, poses significant challenges in early detection and prognostic assessment. Despite advancements in targeted therapies and immunotherapy, the timely identification of relapse remains elusive. Blood-based liquid biopsy biomarkers, including circulating tumor cells (CTCs), cell-free DNA (cfDNA), circulating tumor DNA (ctDNA), circulating-free RNAs (cfRNAs), and extracellular vesicles (EVs)/exosomes, offer promise for non-invasive monitoring. Methods: We employ a comprehensive approach integrating miRNA/lncRNA/metabolomic datasets, following a mixed-methods content analysis, to identify candidate biomarkers in NSCLC. NSCLC-associated miRNA/gene/lncRNA associations were linked to in silico-derived molecular pathways. Results: For data validation, mass spectrometry-based untargeted metabolomics of plasma EVs highlighted miRNA/lncRNA/metabotypes, linking “glycerophospholipid metabolism” to lncRNA H19 and “alanine, aspartate and glutamate metabolism” to miR-29a-3p. Prognostic significance was established for miR-29a-3p, showing lower expression in NSCLC patients with disease progression compared to stable disease (p = 0.004). Kaplan–Meier survival analysis indicated that patients with miR-29a-3p under-expression had significantly shorter overall survival (OS) (p = 0.038). Despite the expression of lncRNA H19 in plasma EVs being undetected, its expression in plasma cfRNAs correlated significantly with disease progression (p = 0.035). Conclusions: Herein, we showcase the potential of plasma EV-derived miR-29a-3p as a prognostic biomarker and underscore the intricate interplay of miRNAs, lncRNAs, and metabolites in NSCLC biology. Our findings offer new insights and avenues for further exploration, contributing to the ongoing quest for effective biomarkers in early-stage NSCLC. Full article
(This article belongs to the Special Issue RNA in Non-Small-Cell Lung Cancer)
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20 pages, 4405 KiB  
Article
Post-Transcriptional Modifications to miRNAs Undergo Widespread Alterations, Creating a Unique Lung Adenocarcinoma IsomiRome
by David E. Cohn, Vanessa G. P. Souza, Aisling Forder, Nikita Telkar, Greg L. Stewart and Wan L. Lam
Cancers 2024, 16(19), 3322; https://doi.org/10.3390/cancers16193322 - 28 Sep 2024
Viewed by 625
Abstract
Background: MicroRNAs (miRNAs) modulate the expression of oncogenes and tumor suppressor genes, functioning as significant epigenetic regulators in cancer. IsomiRs are miRNA molecules that have undergone small modifications during miRNA processing. These modifications can alter an isomiR’s binding stability with mRNA targets, and [...] Read more.
Background: MicroRNAs (miRNAs) modulate the expression of oncogenes and tumor suppressor genes, functioning as significant epigenetic regulators in cancer. IsomiRs are miRNA molecules that have undergone small modifications during miRNA processing. These modifications can alter an isomiR’s binding stability with mRNA targets, and certain isomiRs have been implicated in the development of specific cancers. Still, the isomiRomes of many tissues, including the lung, have not been characterized; Methods: In this study, we analyzed small RNA sequencing data for three cohorts of lung adenocarcinoma (LUAD) and adult non-malignant lung (ANL) samples. Results: We quantified isomiR expression and found 16 A-to-I edited isomiRs expressed in multiple cohorts, as well as 213 5′ isomiRs, 128 3′ adenylated isomiRs, and 100 3′ uridylated isomiRs. Rates of A-to-I editing at editing hotspots correlated with mRNA expression of the editing enzymes ADAR and ADARB1, which were both observed to be deregulated in LUAD. LUAD samples displayed lower overall rates of A-to-I editing and 3′ adenylation than ANL samples. Support vector machines and random forest models were trained on one cohort to distinguish ANL and stage I/II LUAD samples using reads per million (RPM) and frequency data for different types of isomiRs. Models trained on A-to-I editing rates at editing hotspots displayed high accuracy when tested on the other two cohorts and compared favorably to classifiers trained on miRNA expression alone; Conclusions: We have identified isomiRs in the human lung and found that their expression differs between non-malignant and tumor tissues, suggesting they hold potential as cancer biomarkers. Full article
(This article belongs to the Special Issue RNA in Non-Small-Cell Lung Cancer)
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15 pages, 2352 KiB  
Article
A Novel ceRNET Relying on the lncRNA JPX, miR-378a-3p, and Its mRNA Targets in Lung Cancer
by Nicola Mosca, Mariaceleste Pezzullo, Ilenia De Leo, Anna Truda, Giovanna Marchese, Aniello Russo and Nicoletta Potenza
Cancers 2024, 16(8), 1526; https://doi.org/10.3390/cancers16081526 - 17 Apr 2024
Cited by 2 | Viewed by 1428
Abstract
Lung cancer is the leading cause of cancer-related death worldwide. Non-coding RNAs are emerging as critical players for the onset and progression of cancer. Analyses of three different datasets revealed that the lncRNA JPX was overexpressed in adenocarcinoma tissues in comparison to normal [...] Read more.
Lung cancer is the leading cause of cancer-related death worldwide. Non-coding RNAs are emerging as critical players for the onset and progression of cancer. Analyses of three different datasets revealed that the lncRNA JPX was overexpressed in adenocarcinoma tissues in comparison to normal lungs, as expected for an oncogene. Intriguingly, the predicted binding miR-378a-3p showed a significant inverse correlation with JPX expression. The lncRNA/miRNA physical interaction was validated by reporter vectors. Then, the oncogenic activity of JPX, the tumor-suppressive role of miR-378a-3p, and the contribution of their functional interaction to cancer hallmarks were demonstrated using assays for cell proliferation, migration, invasion, and 3D-spheroid formation. Finally, molecular circuits were investigated by boosting the expression of both JPX and miR-378a-3p, singularly and in combination, demonstrating that JPX counteracted miR-378a-3p silencing activity toward its oncogenic targets GLUT1, NRP1, YY1, and Wnt5a. Overall, the data unveil a novel ceRNET (competing endogenous RNA network), wherein JPX acts as a ceRNA by binding to miR-378a-3p, thus reducing the miRNA silencing activity toward its downstream targets, and eliciting oncogenic pathways driving lung cancer. The knowledge of the network may pave the way to develop new diagnostic panels, and innovative RNA-targeted and RNA-based therapeutic strategies. Full article
(This article belongs to the Special Issue RNA in Non-Small-Cell Lung Cancer)
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