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Background: MicroRNA (abbreviated miRNA)-based treatment holds great promise for application as clinical antitumor therapy, but good carriers for delivery of the miRNA drug are lacking. Exosomes secreted by mesenchymal stem cells (MSCs) have proved to be safe, and exogenously modified exosomes may potentially represent an excellent drug delivery vehicle.Methods: In this study, we designed a delivery nano system using single-stranded variable fragment (scFv)-modified exosomes derived from human cord blood MSCs. Genetic engineering technology was used to obtain anti-Glypican 3 (GPC3) scFv-modified exosomes, which were then loaded with miR-26a mimics through electroporation.Results: Results of electron microscopy and dynamic light scattering indicated that the diameter of the drug-carrying exosomes was about 160 nm. Furthermore, anti-GPC3 scFv-modified exosomes effectively delivered miR-26a to GPC3-positive hepatocellular carcinoma cells, thereby inhibiting cell proliferation and migration by regulating the expression of downstream target genes of miR-26a. The exosomes-based nano system displayed favorable anti-tumor effect in vivo with no obvious side effects.Conclusion: Our data provided a new perspective for the use of exosome delivery systems for miRNA-based antitumor therapy.

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Background Glioblastoma (GBM) is an aggressive and malignant brain tumor with extremely poor prognosis. Despite advances in treatment, the pathogenesis of GBM remains elusive. Mounting studies have revealed the critical role of circular RNAs (circRNAs) in the development and progression of human cancers including GBM, but the comprehension of their functions is still insufficient. In this study, we investigated the expression profile of a circRNA derived from GLIS family zinc finger 3 (GLIS3) in GBM and normal astrocytes. CircGLIS3 expression was detected through quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Functional experiments were performed to analyze the influence of circGLIS3 on GBM cell proliferation and apoptosis. In addition, mechanism assays were to uncover the potential regulatory mechanism of circGLIS3. Results CircGLIS3 was up-regulated in GBM cells and knockdown of circGLIS3 significantly hampered proliferation and promoted apoptosis of GBM cells. Furthermore, circGLIS3 positively regulated CAPG and GLIS3 by sponging miR-449c-5p to affect GBM cell proliferation and apoptosis. Conclusions In summary, our study identified that circGLIS3 could promote proliferation and inhibit apoptosis of GBM cells via targeting miR-449c-5p/GLIS3/CAPG axis in vitro. This study could offer a novel molecular perspective for further investigation into mechanisms essential to GBM progression.

Introduction Glioma is the most frequent primary cerebral tumor in adults. Recent evidence has suggested that circular RNAs (circRNAs) are associated with the pathological processes in glioma. In our study, we aimed to investigate the function and mechanism of circ_CAPG (circ_0055412) in glioma. Methods Firstly, circ_0055412 expression was examined through RT‐qPCR analysis. Loss‐of‐function assays and animal experiments were implemented to evaluate the role of circ_0055412 on cisplatin resistance of glioma cells. Moreover, mechanism assays were done to probe into the regulatory mechanism of circ_0055412 in glioma cells. Results Circ_0055412 was found to be notably upregulated in glioma cells. Moreover, depletion of circ_0055412 enhanced cisplatin sensitivity of glioma cells in vitro and in vivo. Moreover, circ_0055412 recruited eukaryotic translation initiation factor 4A3 (EIF4A3) protein to stabilize capping actin protein, gelsolin like (CAPG) mRNA. Furthermore, circ_0055412 served as a sponge for microRNA‐330‐3p (miR‐330‐3p) and regulated nuclear factor of activated T cells 3 (NFATC3) expression to activate the transcription of catenin beta 1 (CTNNB1), thus participating in the activation of Wnt/β‐catenin signaling pathway. Conclusion Circ_0055412 contributed to cisplatin resistance of glioma cells via stabilizing CAPG mRNA and modulating Wnt/β‐catenin signaling pathway. This finding might provide novel information for the treatment of glioma.