miR-1306 Mediates the Feedback Regulation of the TGF-ß/SMAD Signaling Pathway in Granulosa Cells

Yang, Liu; Du, Xing; Liu, Lu; Cao, Qiuyu; Pan, Zengxiang; Li, Qifa

To understand the mechanism by which miR-1306 was up-regulated during follicular atresia, we focused on its transcriptional regulation and promoter region. miR-1306 is transcribed from exon 1 of the porcine DGCR8 gene and suppressed by the transcription factor SMAD4 in porcine GCs [9] . Therefore, we first investigated whether miR-1306 shares a common promoter with its host gene DGCR8. We found that inhibition of SMAD4 significantly raised miR-1306 expression but had no effect on DGCR8 expression in GCs ( Figure 4A ), indicating that miR-1306 has its own promoter and does not share a common promoter with its host gene DGCR8 in porcine GCs. To understand the mechanism by which miR-1306 was up-regulated during follicular atresia, we focused on its transcriptional regulation and promoter region. miR-1306 is transcribed from exon 1 of the porcine DGCR8 gene and suppressed by the transcription factor SMAD4 in porcine GCs [9] . Therefore, we first investigated whether miR-1306 shares a common promoter with its host gene DGCR8. We found that inhibition of SMAD4 significantly raised miR-1306 expression but had no effect on DGCR8 expression in GCs ( Figure 4A ), indicating that miR-1306 has its own promoter and does not share a common promoter with its host gene DGCR8 in porcine GCs.