English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

In the present study, a series of studies were conducted to explore the function of miR-374b in glioma and the regulatory relationship among miR-374b, GATA3 and SEMA3B. In the present study, miR-374b mimics and inhibitors were employed to regulate miR-374b expression. Besides, qRT-PCR assay was used for detecting the expression level of miR-374b, GATA3 and SEMAB mRNAs. To verify the targeting relationship between miR-374b and GATA3, dual luciferase analysis was utilized. Moreover, chromatin immunoprecipitationn (ChIP) assay was performed for identify the correlation of GATA3 with SEMA3B. Furthermore, si1-GATA3, si2-GATA3 and pc-GATA3 were used to regulate GATA3 expression, and pc-SEMA3B was taken advantage for dysregulating SEMA3B. For assessing the significance of miR374b alone or co-operated with GATA3 or SEMA3B in cell viability, migration and apoptosis, CCK-8, transwell and FCM assay were performed, respectively. We found that overexpression of miR-374b, which was identified in glioma tissues and cell lines, U251, LN-299 and GOS-3, promoting cell migration and enhancing cell viability but inhibiting cell apoptosis were suggested in this research. Besides, GATA3 contributed to increase in cell viability and migration and decrease in cell apoptosis targeted by miR-374b as evidenced by dual luciferase assay. Moreover, GATA3 binding to the promoter of SEMA3B involved in regulating SEMA3B was revealed. Further, a series of studies demonstrated that miR-374b targeting GATA3 regulating SMEA3B resulted in elevation in cell viability and migration but suppression in cell apoptosis. But the promotion effects of miR-374 in glioma process were reversed by co-transfecting pc-GATA3 or pc-SEMA3B. In conclusion, miR-374b promotes glioma process in vitro through suppressing SEMA3B via targeting GATA3. The result of this study provides an important clue to the optimal treatment schedule for glioblastoma.

MiR-374b targets GATA3 to promote progression and development of glioblastoma via regulating SEMA3B