MiR-23b-3p reduces the proliferation, migration and invasion of cervical cancer cell lines via the reduction of c-Met expression

Malignant transformation and progression in cancer is associated with the altered expression of multiple miRNAs, which are considered as post-transcriptional regulators of genes participating in various cellular processes. Although, it has been proposed that miR-23b-3p acts as a tumor suppressor in...

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Veröffentlicht in:Scientific reports 2020-02, Vol.10 (1), p.3256-3256, Article 3256
Hauptverfasser: Campos-Viguri, Gabriela Elizabeth, Peralta-Zaragoza, Oscar, Jiménez-Wences, Hilda, Longinos-González, Alma Edith, Castañón-Sánchez, Carlos Alberto, Ramírez-Carrillo, Miriam, Camarillo, César López, Castañeda-Saucedo, Eduardo, Jiménez-López, Marco Antonio, Martínez-Carrillo, Dinorah Nashely, Fernández-Tilapa, Gloria
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Sprache:eng
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Zusammenfassung:Malignant transformation and progression in cancer is associated with the altered expression of multiple miRNAs, which are considered as post-transcriptional regulators of genes participating in various cellular processes. Although, it has been proposed that miR-23b-3p acts as a tumor suppressor in cervical cancer (CC), not all the pathways through which it alters the cellular processes have been described. The present study examines whether miR-23b-3p directly represses the c-Met expression and that consequently modifies the proliferation, migration and invasion of C33A and CaSki cells. c-Met has five microRNA response elements (MREs) for miR-23b-3p in the 3′-UTR region. The ectopic overexpression of miR-23b-3p significantly reduces c-Met expression in C33A and CaSki cells. The overexpression of miR-23b-3p reduces proliferation, migration and invasion of CaSki cells and the proliferation and invasion in C33A cells. In CaSki cells, the activation of Gab1 and Fak, downstream of c-Met, is reduced in response to the overexpression of miR-23b-3p. Together, the results in the present study indicate that miR-23b-3p is a tumor suppressor that modulates the progression of CC via post-transcriptional regulation of the c-Met oncogene.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-020-60143-x