IADR Abstract Archives
MiR-134 Targets PDCD7 to Enhance Oral Carcinogenesis
Objectives: MicroRNA miR-134 was shown to be oncogenic in oral squamous cell carcinoma (OSCC). This study investigated the molecular mechanisms underlying the OSCC pathogenesis associated with miR-134.
Methods: OSCC cells were analyzed following the stimulation or blockage of miR-134, and/or the expression or knockdown of programmed cell death 7 (PDCD7). The expression of miR-134 and PDCD7 in OSCC tumors tissues were also analyzed.
Results: The analysis showed the down-regulation of expression in OSCC cell subclones ectopically expressed miR-134. Whereas, the ectopic miR-134Zip expression up-regulated PDCD7 expression in OSCC cells. Reporter assays confirmed the binding of miR-134 to the wild type 3’un-translated region (3’UTR) of PDCD7, which decreased reporter activity. The targeting of miR-134 to the 3’UTR of PDCD7 was abolished by the mutations in targeted sequences. Furthermore, miR-134Zip expression increased the activity of wild type reporter. Down-regulation of PDCD7 mRNA expression was identified in around 70% of OSCC tumor tissues. A reverse expression between miR-134 and PDCD7 was present in OSCC tumors. Up-regulation of PDCD7 was induced by cisplatin, and PDCD7 expression suppressed the oncogenicity of OSCC cells. Moreover, miR-134 associated cellular transformation and trans-differentiation was attenuated by PDCD7.
Conclusions: This study concludes that the oncogenic potential of miR-134 in oral carcinoma is mediated by targeting PDCD7 suppressor.
Methods: OSCC cells were analyzed following the stimulation or blockage of miR-134, and/or the expression or knockdown of programmed cell death 7 (PDCD7). The expression of miR-134 and PDCD7 in OSCC tumors tissues were also analyzed.
Results: The analysis showed the down-regulation of expression in OSCC cell subclones ectopically expressed miR-134. Whereas, the ectopic miR-134Zip expression up-regulated PDCD7 expression in OSCC cells. Reporter assays confirmed the binding of miR-134 to the wild type 3’un-translated region (3’UTR) of PDCD7, which decreased reporter activity. The targeting of miR-134 to the 3’UTR of PDCD7 was abolished by the mutations in targeted sequences. Furthermore, miR-134Zip expression increased the activity of wild type reporter. Down-regulation of PDCD7 mRNA expression was identified in around 70% of OSCC tumor tissues. A reverse expression between miR-134 and PDCD7 was present in OSCC tumors. Up-regulation of PDCD7 was induced by cisplatin, and PDCD7 expression suppressed the oncogenicity of OSCC cells. Moreover, miR-134 associated cellular transformation and trans-differentiation was attenuated by PDCD7.
Conclusions: This study concludes that the oncogenic potential of miR-134 in oral carcinoma is mediated by targeting PDCD7 suppressor.