Abstract
BackgroundAngiogenesis plays an important role in the progress of glioma. RNA-binding proteins (RBPs) and circular RNAs (circRNAs), dysregulated in various tumors, have been verified to mediate diverse biological behaviors including angiogenesis.MethodsQuantitative real-time PCR (qRT-PCR) and western blot were performed to detect the expression of SRSF10, circ-ATXN1, miR-526b-3p, and MMP2/VEGFA. The potential function of SRSF10/circ-ATXN1/miR-526b-3p axis in glioma-associated endothelial cells (GECs) angiogenesis was further studied.ResultsSRSF10 and circ-ATXN1 were significantly upregulated in GECs compared with astrocyte-associated endothelial cells (AECs). Knockdown of SRSF10 or circ-ATXN1 significantly inhibited cell viability, migration and tube formation of GECs where knockdown of SRSF10 exerted its function by inhibiting the formation of circ-ATXN1. Moreover, the combined knockdown of SRSF10 and circ-ATXN1 significantly enhanced the inhibitory effects on cell viability, migration and tube formation of GECs, compared with knockdown of SRSF10 and circ-ATXN1, respectively. MiR-526b-3p was downregulated in GECs. Circ-ATXN1 functionally targeted miR-526b-3p in an RNA-induced silencing complex. Up-regulation of miR-526b-3p inhibited cell viability, migration and tube formation of GECs. Furthermore, miR-526b-3p affected the angiogenesis of GECs via negatively regulating the expression of MMP2/VEGFA.ConclusionSRSF10/circ-ATXN1/miR-526b-3p axis played a crucial role in regulating the angiogenesis of GECs. The above findings provided new targets for anti-angiogenic therapy in glioma.
Highlights
Angiogenesis plays an important role in the progress of glioma
QRT-PCR was used to detect that expression of both SRSF10 and RNPC1 were elevated in Glioma associated endothelial cells (GEC) with the former being more evident (Supplementary Figure S1B)
We established GECs with downregulated SRSF10 to demonstrate the potential roles of SRSF10 in cell viability
Summary
Angiogenesis plays an important role in the progress of glioma. RNA-binding proteins (RBPs) and circular RNAs (circRNAs), dysregulated in various tumors, have been verified to mediate diverse biological behaviors including angiogenesis. The poor survival of glioma is caused by its abundant angiogenesis, strong invasiveness, and therapeutic resistance [2, 3]. Excessive angiogenesis has become an indicator for glioma growth [4]. Angiogenesis is the process where new vessels arise from existing vessels, participating in a variety of physiological and pathological process. Abnormality in vessel proliferation is necessary for the growth, proliferation and migration of most solid tumors [5]. Investigation into the mechanism of glioma angiogenesis may provide new insights and reveal molecular targets for therapeutic research of glioma
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