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Cancers
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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: 20 August 2025 | Viewed by 1067

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 (2 papers)

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Research

23 pages, 6890 KiB  
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 180
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 KiB  
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 362
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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