The blood-tumor barrier (BTB) restricts the efficient delivery of anti-glioma drugs to cranial glioma tissues.Increased BTB permeability may allow greater delivery of the therapeutic agents.Increasing evidence has revealed that PIWI proteins and PIWI-interacting RNAs (piRNAs) play an important role in tumor progression.
However, whether dr dabber boost evo atomizer replacement PIWI proteins and piRNAs regulate BTB permeability remains unclear.In the present study, we demonstrated that the PIWIL1/piRNA-DQ593109 (piR-DQ593109) complex was the predominant regulator of BTB permeability.Briefly, PIWIL1 was upregulated in glioma endothelial cells (GECs).
Furthermore, piR-DQ593109 was also overexpressed in GECs, as revealed via a piRNA microarray.Downregulation of PIWIL1 or piR-DQ593109 increased the permeability of the BTB.Moreover, PIWIL1 and piR-DQ593109, which formed a piRNA-induced silencing complex, green queen homies degraded the long non-coding RNA maternally expressed 3 (MEG3) in a sequenced-dependent manner.
Furthermore, restoring MEG3 released post-transcriptional inhibition of Runt related transcription factor 3 (RUNX3) by sponging miR-330-5p.In addition, RUNX3 bounded to the promoter regions and reduced the promoter activities of ZO-1, occludin, and claudin-5, which significantly impaired the expression levels of ZO-1, occludin, and claudin-5.In conclusion, downregulating PIWIL1 and piR-DQ593109 increased BTB permeability through the MEG3/miR-330-5p/RUNX3 axis.
These data may provide insight into glioma treatment.