Circ_CLIP2 promotes glioma progression through targeting the miR-195-5p/HMGB3 axis

Background Circular RNA (circRNA) has been demonstrated to play key roles in regulating glioma progression. Understanding the regulatory mechanism of circRNA in glioma is vital to reveal the pathogenesis of glioma and develop novel therapeutic strategies. Therefore, our study focuses on the role and underlying mechanism of Circ_CLIP2 in glioma. Methods The expression of Circ_CLIP2, miR-195-5p and HMGB3 in glioma cells and tissues were analyzed using qRT-PCR. Cell proliferation was determined with colony formation and MTT assays. Cell cycle and apoptosis were examined by flow cytometry. Western blot was conducted for analyzing HMGB3, PCNA, Bax, Bcl-2, cleaved-caspase 3, Wnt-1 and beta-catenin. Dual-luciferase reporter assay was measured to investigate the interaction among Circ_CLIP2, miR-195-5p and HMGB3. Results The expression of Circ_CLIP2 and HMGB3 were increased while miR-195-5p was down-regulated in glioma cells and patients. Silencing of Circ_CLIP2 inhibited cell proliferation, enhanced cell apoptosis and inhibited the Wnt/beta-catenin signaling pathway. Circ_CLIP2 suppressed miR-195-5p expression by directly sponging miR-195-5p. MiR-195-5p inhibited HMGB3 expression via directly targeting HMGB3. Knockdown of miR-195-5p facilitated cell proliferation, inhibited cell apoptosis and activated Wnt/beta-catenin signaling, which were reversed by silencing of HMGB3. Conclusion Knockdown of Circ_CLIP2 suppresses glioma progression by targeting miR-195-5p/HMGB3 thus inhibiting Wnt/beta-catenin signaling. This study may provide potential therapeutic targets against glioma.

Automated summary

The study showed that Circ_CLIP2 and HMGB3 were upregulated while miR-195-5p was downregulated in glioma cells. Silencing of Circ_CLIP2 inhibited cell proliferation and promoted cell apoptosis. MiR-195-5p inhibited HMGB3 expression by directly targeting HMGB3, leading to the suppression of the Wnt/beta-catenin signaling pathway.