MicroRNAs in Cancer Therapy: Recent Advances and Prospects

A special issue of Pharmaceutics (ISSN 1999-4923). This special issue belongs to the section "Gene and Cell Therapy".

Deadline for manuscript submissions: closed (20 January 2025) | Viewed by 1642

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Guest Editor
Center of Molecular Biology and Pharmacogenetics, Department of Basic Sciences, Faculty of Medicine, Universidad de La Frontera, Temuco 4811230, Chile
Interests: pharmacogenomics; pharmacoepigenetics; nanomedicine; toxicity of cancer chemotherapy; biological evaluation of natural compounds; cardiovascular diseases

Special Issue Information

Dear Colleagues,

The abnormal expression of microRNAs (miRNAs), which are regulatory small non-coding RNAs, occurs in pathological events such as cancer. Their extraordinary regulatory potential, which enables the regulation of entire signalling networks within the cells, makes them an interesting tool for the development of cancer therapeutics. The pattern of miRNAs expression can be correlated with the cancer type, stage, and other clinical variables. It has been demonstrated that miRNAs are implicated in almost all aspects of cancer biology, such as proliferation, apoptosis, invasion/metastasis, and angiogenesis. A number of miRNAs affect the growth of cancer cells in vitro and in vivo when overexpressed or inhibited. Therefore, cancer cell growth can be controlled by manipulating miRNAs.

In this Special Issue of Pharmaceutics, original articles and comprehensive reviews that present novel anticancer strategies with a focus on miRNAs exhibting experimentally proven therapeutic potential and that discuss recent advances in the technical development and clinical evaluation of miRNA-based therapeutic agents are welcome. These strategies should address the optimization of cancer therapies that could offer remarkable clinical value in the near future. We therefore encourage the submission of articles that focus on the development and validation of various novel anticancer approaches including, but not limited to, synthetic miRNA mimics such as the siRNA-like oligoribonucleotide duplex or chemically modified oligoribonucleotide, and strategies involving miRNA delivery using liposomes, viral vectors and nanoparticles, among others.

Prof. Dr. Luis A. Salazar
Guest Editor

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Keywords

  • cancer therapy
  • miRNA mimics
  • miRNA delivery
  • oligoribonucleotide
  • siRNA-like oligoribonucleotide
  • drug delivery
  • therapy resistance
  • miRNA antagonists
  • viral vectors
  • LNA-modified oligonucleotides

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Published Papers (1 paper)

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Research

16 pages, 5438 KiB  
Article
miR-195-5p Inhibits Colon Cancer Progression via KRT23 Regulation
by Emanuele Piccinno, Viviana Scalavino, Nicoletta Labarile, Raffaele Armentano, Gianluigi Giannelli and Grazia Serino
Pharmaceutics 2024, 16(12), 1554; https://doi.org/10.3390/pharmaceutics16121554 - 4 Dec 2024
Viewed by 952
Abstract
Background/Objectives: KRT23 was recently discovered as an epithelial-specific intermediate filament protein in the type I keratin family. Many studies have underlined keratin’s involvement in several biological processes as well as in the pathogenesis of different diseases. Specifically, KRT23 was reported to affect the [...] Read more.
Background/Objectives: KRT23 was recently discovered as an epithelial-specific intermediate filament protein in the type I keratin family. Many studies have underlined keratin’s involvement in several biological processes as well as in the pathogenesis of different diseases. Specifically, KRT23 was reported to affect the structural integrity of epithelial cells and to trigger cellular signaling leading to the onset of cancer. The aim of this study is to characterize a novel mechanism based on miR-195-5p/KRT23 in colorectal cancer. Methods: KRT23 mRNA and protein expression were characterized in FFPE sections from patients with CRC. The effects of miR-195-5p on KRT23 expression at the mRNA and protein levels were assessed by transient transfection experiments with mimic and inhibitor molecules. Cell attachment/detachment, migration, invasion, clone formation, and apoptosis were evaluated in human CRC cell lines after miR-195-5p mimic transfection. Results: We identified KRT23 as a putative target of miR-195-5p, a microRNA that we previously demonstrated to be reduced in CRC. We have proved the KRT23 expression deregulation in the tumoral section compared to adjacent normal mucosa in patients with CRC, according to the data derived from the public repository. We proved that the gain of miR-195-5p decreased the KRT23 expression. Conversely, we demonstrated that the inhibition of miR-195-5p led to an increase in KRT23 expression levels. We have demonstrated the in vitro effectiveness of miR-195-5p on CRC progression and that the in vivo intraperitoneal delivery of miR-195-5p mimic lowered colonic KRT23 mRNA and protein expression. Conclusions: These findings highlight a new regulatory mechanism by miR-195-5p in CRC affecting the keratin intermediate filaments and underline the miR-195-5p potential clinical properties. Full article
(This article belongs to the Special Issue MicroRNAs in Cancer Therapy: Recent Advances and Prospects)
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