Silencing of STIM1 Inhibits Epstein-Barr Virus (EBV)-Related Nasopharyngeal Carcinoma Cell Lines Survival by Regulating MIR-200A- 3p and MIR-375 Activities
Keywords:
stromal interaction molecule 1 (STIM1), Dicer substrate short interfering RNA (DsiRNA), EBV-related NPC, miRNAAbstract
Epstein-Barr virus (EBV) infection is associated with many cancers pathogenesis, especially nasopharyngeal cancer (NPC). This infection has been reported to promote metastatic potential via stromal interaction molecule 1 (STIM1). However, the post-transcriptional regulation of STIM1 activities in EBV-related NPC is not well understood yet. This study aims to investigate the post-transcriptional regulatory roles of STIM1 silencing in EBV- related NPC. C666-1 cells is an NPC cell line model harbouring EBV. The C666-1 cells were transfected with Dicer substrate short interfering RNA (DsiRNA) targeting STIM1 for 48 and 72 h periods. The expression of STIM1 and a set of microRNAs were determined via qRT- PCR. The post-translational expressions of RAC1 and CDKN1B proteins were determined via western blot profile. The functional profile of STIM1 silencing showed inhibition of C666-1 cells proliferation and migration activities. Our molecular finding suggests that STIM1 silencing could promote tumor suppressor activities via miR-375 and CDKN1B expression. This study suggests that STIM1 silencing could suppress the survival of EBV- related NPC cells via post-transcriptional regulation of miR-375 and miR-200a-3p as well as post translational regulation of RAC1 and CDKN1B proteins. Further comprehensive work is needed to support this finding especially involving in vivo work.
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