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The Role of MicroRNA in Tumor Development and Treatment

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 3897

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Special Issue Editor

Dr. Paola Campomenosi

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Guest Editor

Dipartimento di Biotecnologie e Scienze della Vita (DBSV), Università degli Studi dell’Insubria, Via Dunant 3, 21100 Varese, Italy
Interests: serum cell free DNA; p53; microRNA

Special Issue Information

Dear Colleagues,

MicroRNAs are small RNA molecules that play important roles in the development of cell and tissue physiology. By regulating gene expression—mainly at the post-transcriptional level—these molecules influence all aspects of cell life, ranging from proliferation to apoptosis, cell growth arrest, differentiation and migration. MicroRNAs are pleiotropic: each microRNA can regulate the expression of hundreds of genes. Differences in the types and abundance of transcripts in each cell type will influence the outcomes generated by specific microRNAs in the different cell types. MicroRNAs are also present in extracellular vesicles and thus mediate cell–cell signaling in addition to having autocrine effects.

Importantly, alterations in microRNAs occur in several types of pathologies, including cardiovascular diseases, neurodegenerative disorders and cancer. In cancer, microRNAs influence all aspects of tumor cell growth and also how tumors respond to therapy.

We welcome researchers to submit articles and reviews to this Special Issue, entitled “The Role of MicroRNA in Tumor Development and Treatment”. These should deal with the mechanisms by which microRNAs influence tumor development, responses to treatment, the onset of drug resistance and the methods by which microRNAs may be exploited for cancer therapy.

Dr. Paola Campomenosi
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 short 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

microRNA
microRNA function
regulation of gene expression
tumor development
cancer treatment
drug resistance

Published Papers (3 papers)

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Research

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15 pages, 2684 KiB

Open AccessArticle

Let-7a Downregulation Accompanied by KRAS Mutation Is Predictive of Lung Cancer Onset in Cigarette Smoke–Exposed Mice

by Alessandra Pulliero, Luca Mastracci, Letizia Tarantini, Zumama Khalid, Valentina Bollati and Alberto Izzotti

Int. J. Mol. Sci. 2023, 24(14), 11778; https://doi.org/10.3390/ijms241411778 - 21 Jul 2023

Cited by 2 | Viewed by 1332

Abstract

Background: Let-7 is a tumor suppressor microRNA targeting the KRAS lung oncogene. Let-7a downregulation is reversible during the early stages of lung carcinogenesis but is irreversible in cancer cells. The aim of this study is to shed light on the relationship between oncogene (KRAS) mutation and let-7a downregulation in cigarette smoke (CS)-induced lung carcinogenesis. Methods: A total of 184 strain H Swiss albino mice were either unexposed (control) or exposed to CS for 2 weeks (short CS) or 8 months (long CS). After 8 months, the lungs were individually collected. The following end points have been evaluated: (a) DNA methylation of the let-7a gene promoter by bisulphite-PCR and pyrosequencing; (b) let-7a expression by qPCR; (c) KRAS mutation by DNA pyrosequencing; (d) cancer incidence by histopathological examination. Results: let-7a expression decreased by 8.3% in the mice exposed to CS for two weeks (CS short) and by 33.4% (p ≤ 0.01) in the mice exposed to CS for 8 months (CS long). No significant difference was detected in the rate of let-7a-promoter methylation between the Sham-exposed mice (55.1%) and the CS short-(53%) or CS long (51%)-exposed mice. The percentage of G/T transversions in KRAS codons 12 and 13 increased from 2.3% (Sham) to 6.4% in CS short– and to 11.5% in CS long–exposed mice. Cancer incidence increased significantly in the CS long–exposed mice (11%) as compared to both the Sham (4%) and the CS short–exposed (2%) mice. In the CS long–exposed mice, the correlation between let-7a expression and the number of KRAS mutations was positive (R = +0.5506) in the cancer-free mice and negative (R = −0.5568) in the cancer-bearing mice. Conclusions: The effects of CS-induced mutations in KRAS are neutralized by the high expression of let-7a in cancer-free mice (positive correlation) but not in cancer-bearing mice where an irreversible let-7a downregulation occurs (negative correlation). This result provides evidence that both genetic (high load of KRAS mutation) and epigenetic alterations (let-7a irreversible downregulation) are required to produce lung cancer in CS-exposed organisms. Full article

(This article belongs to the Special Issue The Role of MicroRNA in Tumor Development and Treatment)

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Review

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18 pages, 1470 KiB

Open AccessReview

The Role of miRNAs to Detect Progression, Stratify, and Predict Relevant Clinical Outcomes in Bladder Cancer

by Maria Iyali Torres-Bustamante, Jorge Raul Vazquez-Urrutia, Fabiola Solorzano-Ibarra and Pablo Cesar Ortiz-Lazareno

Int. J. Mol. Sci. 2024, 25(4), 2178; https://doi.org/10.3390/ijms25042178 - 11 Feb 2024

Viewed by 724

Abstract

Bladder cancer (BC) is one of the most common types of cancer worldwide, with significant differences in survival depending on the degree of muscle and surrounding tissue invasion. For this reason, the timely detection and monitoring of the disease are important. Surveillance cystoscopy is an invasive, costly, and uncomfortable procedure to monitor BC, raising the need for new, less invasive alternatives. In this scenario, microRNAs (miRNAs) represent attractive prognostic tools given their role as gene regulators in different biological processes, tissue expression, and their ease of evaluation in liquid samples. In cancer, miRNA expression is dynamically modified depending on the tumor type and cancer staging, making them potential biomarkers. This review describes the most recent studies in the last five years exploring the utility of miRNA-based strategies to monitor progression, stratify, and predict relevant clinical outcomes of bladder cancer. Several studies have shown that multimarker miRNA models can better predict overall survival, recurrence, and progression in BC patients than traditional strategies, especially when combining miRNA expression with clinicopathological variables. Future studies should focus on validating their use in different cohorts and liquid samples. Full article

(This article belongs to the Special Issue The Role of MicroRNA in Tumor Development and Treatment)

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18 pages, 1932 KiB

Open AccessReview

The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development

by Ekaterina Isachesku, Cornelia Braicu, Radu Pirlog, Anja Kocijancic, Constantin Busuioc, Lavinia-Lorena Pruteanu, Deo Prakash Pandey and Ioana Berindan-Neagoe

Int. J. Mol. Sci. 2023, 24(22), 16320; https://doi.org/10.3390/ijms242216320 - 14 Nov 2023

Cited by 1 | Viewed by 1337

Abstract

Glioblastoma (GBM) is a primary brain tumor arising from glial cells. The tumor is highly aggressive, the reason for which it has become the deadliest brain tumor type with the poorest prognosis. Like other cancers, it compromises molecular alteration on genetic and epigenetic levels. Epigenetics refers to changes in gene expression or cellular phenotype without the occurrence of any genetic mutations or DNA sequence alterations in the driver tumor-related genes. These epigenetic changes are reversible, making them convenient targets in cancer therapy. Therefore, we aim to review critical epigenetic dysregulation processes in glioblastoma. We will highlight the significant affected tumor-related pathways and their outcomes, such as regulation of cell cycle progression, cell growth, apoptosis, angiogenesis, cell invasiveness, immune evasion, or acquirement of drug resistance. Examples of molecular changes induced by epigenetic modifications, such as DNA epigenetic alterations, histone post-translational modifications (PTMs), and non-coding RNA (ncRNA) regulation, are highlighted. As understanding the role of epigenetic regulators and underlying molecular mechanisms in the overall pro-tumorigenic landscape of glioblastoma is essential, this literature study will provide valuable insights for establishing the prognostic or diagnostic value of various non-coding transcripts, including miRNAs. Full article

(This article belongs to the Special Issue The Role of MicroRNA in Tumor Development and Treatment)

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