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Hsa-miR-183-5p modulates cell adhesion by repression of ITGB1 expression in prostate cancer

Prostate cancer is a major health problem worldwide. MiR-183 is an oncomiR and a candidate biomarker in prostate cancer, affecting various pathways responsible for disease initiation and progression. We sought to discover the most relevant processes controlled by miR-183 through an unbiased transcri...

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Main Author: Oliveira-Rizzo, Carolina (author)
Other Authors: Ottati Braselli, María Carolina (author), Fort Canobra, Rafael S (author), Chávez, Santiago (author), Trinidad Barnech, Juan Manuel (author), Di Paolo, Andrés (author), Garat, Beatriz (author), Sotelo-Silveira, José Roberto (author), Duhagon, María Ana (author)
Format: article
Language:English
Published: 2022
Subjects:
Cancer
MicroRNA
Focal adhesion
miR-183
Prostate
ITGB
TCGA
AGO-PAR-CLIP
Online Access:https://hdl.handle.net/20.500.12008/41376
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Summary:Prostate cancer is a major health problem worldwide. MiR-183 is an oncomiR and a candidate biomarker in prostate cancer, affecting various pathways responsible for disease initiation and progression. We sought to discover the most relevant processes controlled by miR-183 through an unbiased transcriptomic approach using prostate cell lines and patient tissues to identify miR-183 responsive genes and pathways. Gain of unction experiments, reporter gene assays, and transcript and protein measurements were conducted to validate predicted functional effects and protein mediators. A total of 135 candidate miR-183 target genes overrepresenting cell adhesion terms were inferred from the integrated transcriptomic analysis. Cell attachment, spreading assays and focal adhesion quantification of miR-183-overexpressing cells confirmed the predicted reduction in cell adhesion. ITGB1 was validated as a major target of repression by miR-183 as well as a mediator of cell adhesion in response to miR-183. The reporter gene assay and PAR-CLIP read mapping suggest that ITGB1 may be a direct target of miR-183. The negative correlation between miR-183 and ITGB1 expression in prostate cancer cohorts supports their interaction in the clinical set. Overall, cell adhesion was uncovered as a major pathway controlled by miR-183 in prostate cancer, and ITGB1 was identified as a relevant mediator of this effect.

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