MiR-21 Regulates Growth and Migration of Cervical Cancer Cells by RECK Signaling Pathway.
Seidy Y Aguilar-MartínezGabriela E Campos-ViguriSelma E Medina-GarcíaRicardo J García-FloresJessica DeasClaudia Gómez-CerónAbraham Pedroza-TorresElizabeth BautistaGloria Fernández-TilapaMauricio Rodríguez-DorantesCarlos Perez-PlasenciaOscar Peralta-ZaragozaPublished in: International journal of molecular sciences (2024)
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.
Keyphrases
- cell proliferation
- long non coding rna
- poor prognosis
- long noncoding rna
- cell cycle
- pi k akt
- signaling pathway
- gene expression
- young adults
- stem cells
- cell migration
- genome wide
- epithelial mesenchymal transition
- risk assessment
- oxidative stress
- multidrug resistant
- crispr cas
- copy number
- mesenchymal stem cells
- cell cycle arrest