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Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for...
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Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for Diagnosis and Therapy

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

Deadline for manuscript submissions: 28 February 2026 | Viewed by 3607

Special Issue Editors

Dr. Amog Urs

E-Mail Website
Guest Editor
Division of Hematology and Hematological Malignancies, Huntsman Cancer Institute, University of Utah Health, Salt Lake City, UT, USA
Interests: leukemia; long non-coding RNA; circular RNA; hematopoietic stem cells; transplantation; xenograft
Special Issues, Collections and Topics in MDPI journals
Dr. Udhayakumar Gopal

E-Mail Website
Guest Editor
Division of Hematology and Hematological Malignancies, Huntsman Cancer Institute, University of Utah Health, Salt Lake City, UT, USA
Interests: cancer biology; chronic myelomonocytic leukemia (CMML); signaling pathways in metastasis; metabolism and transcriptome; zebrafish model

Special Issue Information

Dear Colleagues,

This Special Issue aims to consolidate current research on the identification and characterization of non-coding RNA (ncRNA) signatures in various cancers. Non-coding RNAs, including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), play crucial roles in the regulation of gene expression and have been implicated in cancer pathogenesis, diagnosis and treatment. We welcome original research articles, reviews and communications that cover these aspects. Additionally, we encourage submissions that investigate the underlying mechanisms by which ncRNAs influence cancer progression and response to treatment.

Dr. Amog Urs
Dr. Udhayakumar Gopal
Guest Editors

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

  • non-coding RNA
  • biomarkers
  • gene regulation
  • microRNA
  • long non-coding RNA
  • circular RNA
  • therapeutic targets

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Published Papers (5 papers)

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Research

Jump to: Review

20 pages, 3941 KB  
Article
MicroRNA Expression Analysis and Biological Pathways in Chemoresistant Non-Small Cell Lung Cancer
by Chara Papadaki, Maria Mortoglou, Aristeidis E. Boukouris, Krystallia Gourlia, Maria Markaki, Eleni Lagoudaki, Anastasios Koutsopoulos, Ioannis Tsamardinos, Dimitrios Mavroudis and Sofia Agelaki
Cancers 2025, 17(15), 2504; https://doi.org/10.3390/cancers17152504 - 29 Jul 2025
Viewed by 608
Abstract
Background/Objectives: Alterations in DNA damage repair mechanisms can impair the therapeutic effectiveness of cisplatin. MicroRNAs (miRNAs), key regulators of DNA damage repair processes, have been proposed as promising biomarkers for predicting the response to platinum-based chemotherapy (CT) in non-small cell lung cancer (NSCLC). [...] Read more.
Background/Objectives: Alterations in DNA damage repair mechanisms can impair the therapeutic effectiveness of cisplatin. MicroRNAs (miRNAs), key regulators of DNA damage repair processes, have been proposed as promising biomarkers for predicting the response to platinum-based chemotherapy (CT) in non-small cell lung cancer (NSCLC). In this study, by using a bioinformatics approach, we identified six miRNAs, which were differentially expressed (DE) between NSCLC patients characterized as responders and non-responders to platinum-based CT. We further validated the differential expression of the selected miRNAs on tumor and matched normal tissues from patients with resected NSCLC. Methods: Two miRNA microarray expression datasets were retrieved from the Gene Expression Omnibus (GEO) repository, comprising a total of 69 NSCLC patients (N = 69) treated with CT and annotated data from their response to treatment. Differential expression analysis was performed using the Linear Models for Microarray Analysis (Limma) package in R to identify DE miRNAs between responders (N = 33) and non-responders (N = 36). Quantitative real-time PCR (qRT-PCR) was used to assess miRNA expression levels in clinical tissue samples (N = 20). Results: Analysis with the Limma package revealed 112 DE miRNAs between responders and non-responders. A random-effects meta-analysis further identified 24 miRNAs that were consistently up- or downregulated in at least two studies. Survival analysis using the Kaplan–Meier plotter (KM plotter) indicated that 22 of these miRNAs showed significant associations with prognosis in NSCLC. Functional and pathway enrichment analysis revealed that several of the identified miRNAs were linked to key pathways implicated in DNA damage repair, including the p53, Hippo, PI3K and TGF-β signaling pathways. We finally distinguished a six-miRNA signature consisting of miR-26a, miR-29c, miR-34a, miR-30e-5p, miR-30e-3p and miR-497, which were downregulated in non-responders and are involved in at least three DNA damage repair pathways. Comparative expression analysis on tumor and matched normal tissues from surgically treated NSCLC patients confirmed their differential expression in clinical samples. Conclusions: In summary, we identified a signature of six miRNAs that are suppressed in NSCLC and may serve as a predictor of cisplatin response in NSCLC. Full article
(This article belongs to the Special Issue Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for Diagnosis and Therapy)
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23 pages, 6890 KB  
Article
MicroRNA Signatures in Lung Adenocarcinoma Metastases: Exploring the Oncogenic Targets of Tumor-Suppressive miR-195-5p and miR-195-3p
by Yuya Tomioka, Naohiko Seki, Keiko Mizuno, Takayuki Suetsugu, Kentaro Tsuruzono, Yoko Hagihara, Mayuko Kato, Chikashi Minemura, Hajime Yonezawa, Kentaro Tanaka and Hiromasa Inoue
Cancers 2025, 17(14), 2348; https://doi.org/10.3390/cancers17142348 - 15 Jul 2025
Viewed by 626
Abstract
Background: To improve the prognosis of patients with lung adenocarcinoma (LUAD), revolutionary treatments for metastatic lesions are essential. Methods: To identify genes closely involved in LUAD-cell-derived metastasis, we used RNA sequencing to generate microRNA (miRNA) expression signatures of brain metastatic lesions. [...] Read more.
Background: To improve the prognosis of patients with lung adenocarcinoma (LUAD), revolutionary treatments for metastatic lesions are essential. Methods: To identify genes closely involved in LUAD-cell-derived metastasis, we used RNA sequencing to generate microRNA (miRNA) expression signatures of brain metastatic lesions. Once tumor-suppressive miRNAs are identified, it will be possible to explore the numerous tumor-promoting genes that are regulated by miRNAs. Results: By comparison with a previously created LUAD signature, we identified several miRNAs whose expression was significantly suppressed in brain metastases. We focused on both strands of pre-miR-195 (miR-195-5p and miR-195-3p), which were significantly downregulated in brain metastatic tissues, and confirmed by ectopic expression assays that both strands of pre-miR-195 attenuated the aggressive phenotypes (cell proliferation, migration, and invasion) of LUAD cells. These data suggest that both strands of pre-miR-195 have tumor-suppressive functions in LUAD cells. Next, we explored the target molecules that each miRNA strand regulates in LUAD cells. We identified 159 target genes regulated by miR-195-5p and miR-195-3p, of which 12 genes (ANLN, CDC6, CDCA2, CDK1, CEP55, CHEK1, CLSPN, GINS1, KIF23, MAD2L1, OIP5, and TIMELESS) affect cell cycle/cell division and the prognosis of LUAD patients. Finally, we focused on two genes, ANLN (miR-195-5p target) and MAD2L1 (miR-195-3p target), and demonstrated their oncogenic functions and the molecular pathways they regulate in LUAD cells. Conclusions: The miRNA signature derived from lung cancer brain metastasis will be a landmark in the field, and analysis of this miRNA signature will accelerate the identification of genes involved in lung cancer brain metastasis. Full article
(This article belongs to the Special Issue Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for Diagnosis and Therapy)
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16 pages, 1490 KB  
Article
Mir-16 Decreases the Expression of VTI1B and SMPD1, Genes Involved in Membrane-Protein Trafficking in Melanoma
by Adi Layani, Tal Meningher, Yechezkel Sidi, Dror Avni and Raya Leibowitz
Cancers 2025, 17(13), 2197; https://doi.org/10.3390/cancers17132197 - 29 Jun 2025
Viewed by 634
Abstract
Introduction: The interface between T cells and the tumor microenvironment, termed the ‘immunological synapse’, consists of multiple checkpoint protein pairs co-expressed on both sides of the synapse. mir-16, a microRNA from a widely known tumor-suppressor family of miRNAs, was previously shown by us [...] Read more.
Introduction: The interface between T cells and the tumor microenvironment, termed the ‘immunological synapse’, consists of multiple checkpoint protein pairs co-expressed on both sides of the synapse. mir-16, a microRNA from a widely known tumor-suppressor family of miRNAs, was previously shown by us to be downregulated in melanoma. As other miRNAs from this family have been shown to directly target checkpoint proteins, here we investigated whether miR-16 influences the expression patterns of checkpoint proteins in melanoma. Methods: Single-cell gene expression data from the melanoma microenvironment were retrieved from a public database. Melanoma cell lines were established from metastatic lesions and transiently transfected with an hsa-miR-16-5p-mimic RNA or a mir-16-expressing plasmid. The mRNA expression profiles were analyzed using an Affymetrix microarray. Direct targets of miR-16 were identified by luciferase reporter assays. Protein levels were assessed by Western blotting. Results: Bioinformatic analysis revealed that the expression levels of eight checkpoint mRNAs, known to be present on the melanoma side of the immunological synapse, were highly correlated. Four of these mRNAs contained putative binding sites for the miR-15/16 family. miR-16 expression was significantly reduced in melanoma cells, compared to normal melanocytes. Luciferase reporter assays demonstrated that miR-16 directly targets the 3′ untranslated regions (3′UTRs) of CD40, CD80. The mRNAs downregulated following miR-16 overexpression were highly enriched for genes involved in autophagy, vesicle-mediated transport, and the regulation of protein membrane localization. Among these, VTI1B and SMPD1 were confirmed to be direct targets of miR-16. Transient overexpression of miR-16 resulted in a significant reduction in SMPD1 and VTI1B levels in melanoma cell lines. Conclusions: Our findings suggest that miR-16 potentially modulates melanoma tumorigenesis, metastasis and immunogenicity by altering the composition of checkpoint proteins at the immunological synapse and by regulating cellular pathways associated with intracellular trafficking and transmembrane protein presentation. Full article
(This article belongs to the Special Issue Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for Diagnosis and Therapy)
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Review

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25 pages, 1480 KB  
Review
Functional Heterogeneity and Context-Dependent Roles of LncRNAs in Breast Cancer
by Shu Hui Lye, Nunaya Polycarp, Titilayomi Juliet Durojaye and Trygve O. Tollefsbol
Cancers 2025, 17(19), 3191; https://doi.org/10.3390/cancers17193191 - 30 Sep 2025
Viewed by 335
Abstract
As with other non-coding RNAs (ncRNAs), the aberrant expression of long non-coding RNAs (lncRNAs) can be associated with different forms of cancers, including breast cancer (BC). Various lncRNAs may either promote or suppress cell proliferation, metastasis, and other related cancer signaling pathways by [...] Read more.
As with other non-coding RNAs (ncRNAs), the aberrant expression of long non-coding RNAs (lncRNAs) can be associated with different forms of cancers, including breast cancer (BC). Various lncRNAs may either promote or suppress cell proliferation, metastasis, and other related cancer signaling pathways by interacting with other cellular machinery, thus affecting the expression of BC-related genes. However, lncRNAs are characterized by features that are unlike protein-coding genes, which pose unique challenges when it comes to their study and utility. They are highly diverse and may display contradictory functions depending on factors like the BC subtype, isoform diversity, epigenetic regulation, subcellular localization, interactions with various molecular partners, and the tumor microenvironment (TME), which contributes to the intratumoral heterogeneity and phenotypic plasticity. While lncRNAs have potential clinical utility, their functional heterogeneity coupled with a current paucity of knowledge of their functions present challenges for clinical translation. Strategies to address this heterogeneity include improving classification systems, employing CRISPR/Cas tools for functional studies, utilizing single-cell and spatial sequencing technologies, and prioritizing robust targets for therapeutic development. A comprehensive understanding of the lncRNA functional heterogeneity and context-dependent behavior is crucial for advancing BC research and precision medicine. This review discusses the sources of lncRNA heterogeneity, their implications in BC biology, and approaches to resolve knowledge gaps in order to harness lncRNAs for clinical applications. Full article
(This article belongs to the Special Issue Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for Diagnosis and Therapy)
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30 pages, 530 KB  
Review
DNA Damage and Repair in Ovarian Cancer: Focus on MicroRNAs
by Katarzyna D. Arczewska and Agnieszka Piekiełko-Witkowska
Cancers 2025, 17(18), 3011; https://doi.org/10.3390/cancers17183011 - 15 Sep 2025
Viewed by 747
Abstract
Ovarian cancer (OvCa) is one of the most life-threatening female malignancies that affects 300,000 women annually worldwide. Impaired mechanisms of DNA repair are the leading cause of mutations underlying the OvCa development. microRNAs are short non-coding RNAs that regulate the expression of genes [...] Read more.
Ovarian cancer (OvCa) is one of the most life-threatening female malignancies that affects 300,000 women annually worldwide. Impaired mechanisms of DNA repair are the leading cause of mutations underlying the OvCa development. microRNAs are short non-coding RNAs that regulate the expression of genes by binding to their transcripts and inducing mRNA degradation or inhibition of translation. Here, we review the miRNA-mediated dysregulation of genes involved in DNA damage response (DDR) and DNA repair pathways in OvCa. Apparently, miRNAs are capable of targeting the crucial mediators of DDR (e.g., miR-203a-3p targeting ATM (Ataxia Telangiectasia Mutated)), homologous repair (such as BRCA1 targeted by miR-9, miR-1255b, miR-193b, and miR-148b), non-homologous end joining (with RNF8 being regulated by miR-214), nucleotide excision repair (involving DDB2 targeted by miR-328-3p), or translesion DNA synthesis (involving RAD18, participating also in homologous repair and targeted by miR-379-5p). We also discuss miRNAs (such as miR-519a-3p, let-7e, miR-216b), which affect responses to OvCa therapy by targeting PARP1 (Poly(ADP-Ribose) Polymerase-1). Finally, we also discuss why, despite the identification of multiple miRNAs capable of regulating DNA repair genes, as well as those involved in the response to therapy, no miRNA-based drugs have been approved for OvCa treatment in clinics. Full article
(This article belongs to the Special Issue Exploring Non-Coding RNA Signatures in Cancer: Definitions and Implications for Diagnosis and Therapy)
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