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© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Simple Summary

Previous studies have indicated that the presence of cancer stem cells may be a contributing factor to the development of metastasis in colorectal cancer patients. Cancer stem cells represent a small subpopulation within the tumor mass that exhibits heightened resistance to treatment and possesses the capacity for self-replication, epithelial–mesenchymal transition, and the generation of new tumors. The tumor microenvironment secretes and releases several molecules that facilitate the self-renewal of cancer stem cells and provide support for colorectal cancer progression. microRNAs are involved in direct cell-to-cell signaling and paracrine signaling between tumor cells and other tumor microenvironment components. They could act as tumor suppressors or oncomiRs, and their deregulation is involved in colorectal cancer progression and cancer stem cell formation. In our previous studies, we demonstrated the oncosuppressive function of miR-486-5p in colorectal cancer; these findings prompted us to conduct a more detailed investigation into its role in cancer stem cell phenotypes.

Abstract

Background: Colorectal cancer (CRC) is the third diagnosed cancer worldwide. Forty-four percent of metastatic colorectal cancer patients were diagnosed at an early stage. Despite curative resection, approximately 40% of patients will develop metastases within a few years. Previous studies indicate the presence of cancer stem cells (CSCs) and their contribution to CRC progression and metastasis. miRNAs deregulation plays a role in CSCs formation and in tumor development. In light of previous studies, we investigated the role of miR-486-5p to understand its role in CSC better. Methods: The expression of miR-486-5p was assessed in adherent cells and spheres generated from two CRC cell lines to observe the difference in expression in CSC-enriched spheroids. Afterward, we overexpressed and underexpressed this miRNA in adherent and sphere cultures through the transfection of a miR-486-5p mimic and a mimic inhibitor. Results: The results demonstrated that miR-486-5p exhibited a notable downregulation in CSC models, and its overexpression led to a significant decrease in colony size. Conclusions: In this study, we confirmed that miR-486-5p plays an oncosuppressive role in CRC, thereby advancing our understanding of the role of this microRNA in the CSC phenotype.

Details

Title
The Role of miR-486-5p on CSCs Phenotypes in Colorectal Cancer
Author
Etzi, Federica 1   VIAFID ORCID Logo  ; Griñán-Lisón, Carmen 2   VIAFID ORCID Logo  ; Fenu, Grazia 1   VIAFID ORCID Logo  ; González-Titos, Aitor 3   VIAFID ORCID Logo  ; Pisano, Andrea 1   VIAFID ORCID Logo  ; Farace, Cristiano 1   VIAFID ORCID Logo  ; Sabalic, Angela 1   VIAFID ORCID Logo  ; Picon-Ruiz, Manuel 4   VIAFID ORCID Logo  ; Marchal, Juan Antonio 4   VIAFID ORCID Logo  ; Madeddu, Roberto 5   VIAFID ORCID Logo 

 Department of Biomedical Science, University of Sassari, 07100 Sassari, Italy or [email protected] (F.E.); [email protected] (G.F.); [email protected] (C.F.); [email protected] (A.S.); [email protected] (R.M.) 
 Department of Biochemistry and Molecular Biology 2, Faculty of Pharmacy, University of Granada, Campus de Cartuja s/n, 18071 Granada, Spain; Centre for Genomics and Oncological Research, GENYO, Pfizer/University of Granada/Andalusian Regional Government, 18016 Granada, Spain; Instituto de Investigación Biosanitaria ibs.GRANADA, University Hospitals of Granada, University of Granada, 18012 Granada, Spain; [email protected] (A.G.-T.); [email protected] (M.P.-R.); [email protected] (J.A.M.); Excellence Research Unit “Modeling Nature” (MNat), University of Granada, 18100 Granada, Spain 
 Instituto de Investigación Biosanitaria ibs.GRANADA, University Hospitals of Granada, University of Granada, 18012 Granada, Spain; [email protected] (A.G.-T.); [email protected] (M.P.-R.); [email protected] (J.A.M.); Biopathology and Regenerative Medicine Institute (IBIMER), Centre for Biomedical Research (CIBM), University of Granada, 18100 Granada, Spain 
 Instituto de Investigación Biosanitaria ibs.GRANADA, University Hospitals of Granada, University of Granada, 18012 Granada, Spain; [email protected] (A.G.-T.); [email protected] (M.P.-R.); [email protected] (J.A.M.); Excellence Research Unit “Modeling Nature” (MNat), University of Granada, 18100 Granada, Spain; Biopathology and Regenerative Medicine Institute (IBIMER), Centre for Biomedical Research (CIBM), University of Granada, 18100 Granada, Spain; Department of Human Anatomy and Embryology, Faculty of Medicine, University of Granada, 18016 Granada, Spain 
 Department of Biomedical Science, University of Sassari, 07100 Sassari, Italy or [email protected] (F.E.); [email protected] (G.F.); [email protected] (C.F.); [email protected] (A.S.); [email protected] (R.M.); National Institute of Biostructures and Biosystems, 00136 Rome, Italy 
First page
4237
Publication year
2024
Publication date
2024
Publisher
MDPI AG
e-ISSN
20726694
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
3149547172
Copyright
© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.