Author:
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
Abstract
AbstractMalignant 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.
Funder
Consejo Nacional de Ciencia y Tecnología
Publisher
Springer Science and Business Media LLC
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