| Autor: |
Aguilar-Martínez SY; Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico., Campos-Viguri GE; Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico., Medina-García SE; Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico., García-Flores RJ; Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico., Deas J; Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico., Gómez-Cerón C; Department of Epidemiology of Cancer, Research Center Population Health, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico., Pedroza-Torres A; Programa Investigadoras e Investigadores por México, Consejo Nacional de Humanidades, Ciencias y Tecnologías, México City 14080, Mexico.; Hereditary Cancer Clinic, Instituto Nacional de Cancerología, México City 14080, Mexico., Bautista-Rodríguez E; Clinical Chemistry, Faculty of Health Sciences, Universidad Autónoma de Tlaxcala, Zacatelco 90750, Mexico., Fernández-Tilapa G; Clinical Research Laboratory, Faculty of Chemical Biological Sciences, Universidad Autónoma de Guerrero, Chilpancingo 39070, Mexico., Rodríguez-Dorantes M; Oncogenomics Laboratory, Instituto Nacional de Medicina Genómica, Tlalpan, México City 14610, Mexico., Pérez-Plasencia C; Oncogenomics Laboratory, Instituto Nacional de Cancerología, México City 14080, Mexico.; Biomedicine Unit, FES-Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla de Baz 54090, Mexico., Peralta-Zaragoza O; Direction of Chronic Infections and Cancer, Research Center in Infection Diseases, Instituto Nacional de Salud Pública, Cuernavaca 62100, Mexico. |
| Abstrakt: |
Expression of miR-21 has been found to be altered in almost all types of cancers, and it has been classified as an oncogenic microRNA. In addition, the expression of tumor suppressor gene RECK is associated with miR-21 overexpression in high-grade cervical lesions. In the present study, we analyze the role of miR-21 in RECK gene regulation in cervical cancer cells. To identify the downstream cellular target genes of upstream miR-21, we silenced endogenous miR-21 expression using siRNAs. We analyzed the expression of miR-21 and RECK, as well as functional effects on cell proliferation and migration. We found that in cervical cancer cells, there was an inverse correlation between miR-21 expression and RECK mRNA and protein expression. SiRNAs to miR-21 increased luciferase reporter activity in construct plasmids containing the RECK-3'-UTR microRNA response elements MRE21-1, MRE21-2, and MRE21-3. The role of miR-21 in cell proliferation was also analyzed, and cancer cells transfected with siRNAs exhibited a markedly reduced cell proliferation and migration. Our findings indicate that miR-21 post-transcriptionally down-regulates the expression of RECK to promote cell proliferation and cell migration inhibition in cervical cancer cell survival. Therefore, miR-21 and RECK may be potential therapeutic targets in gene therapy for cervical cancer. |
