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Molecular mechanism of microRNA-26a regulation of phosphatase and tensin homolog gene in condyloma acuminatum and penile squamous cell carcinoma

OBJECTIVE: To investigate the expression levels and mechanisms of microRNA (miRNA) 26a (miR-26a) and phosphatase and tensin homolog (PTEN) in patients with human papillomavirus (HPV)-induced condyloma acuminatum (CA) and penile squamous cell carcinoma (PSCC). METHODS: Thirty-one patients with HPV-po...

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Detalles Bibliográficos
Autores principales: Hu, Yayu, Hu, Enping, Su, Xiangchuan, Chen, Xiangen, Tao, Xiulin, Ren, Xiaoli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267046/
https://www.ncbi.nlm.nih.gov/pubmed/34232796
http://dx.doi.org/10.1177/03000605211014379
Descripción
Sumario:OBJECTIVE: To investigate the expression levels and mechanisms of microRNA (miRNA) 26a (miR-26a) and phosphatase and tensin homolog (PTEN) in patients with human papillomavirus (HPV)-induced condyloma acuminatum (CA) and penile squamous cell carcinoma (PSCC). METHODS: Thirty-one patients with HPV-positive CA and 28 with HPV-positive PSCC were included in this retrospective, cross-sectional study. PTEN mRNA and miR-26a levels in lesion tissues, blood, and urine were analyzed by quantitative reverse transcription polymerase chain reaction, and PTEN protein was detected by western blot and enzyme-linked immunosorbent assay. Cell proliferation was assessed by MTT assay. The interaction between miR-26a and PTEN was predicted by bioinformatics analysis and confirmed by dual luciferase reporter assay RESULTS: PTEN mRNA and protein levels were significantly lower and miR-26a levels were significantly higher in all samples from patients with PSCC compared with the CA group. Bioinformatics analysis and luciferase reporter assay confirmed PTEN as a target gene of miR-26a. Up-regulation of miR-26a significantly increased the proliferation of Penl1 PSCC cells. CONCLUSIONS: PTEN expression is down-regulated and miR-26a levels are up-regulated in PSCC compared with CA. PTEN is a direct target gene of miR-26a. These results suggest that miR-26a might regulate HPV-positive progression from CA to PSCC through modulating PTEN.