Abstract
Currently, miR-21 and CXCR4 are being extensively investigated as two key regulators in glioma malignancy. In this study, we investigated the combined effects of these two factors on glioma progression. Herein, the expression of miR-21 and CXCR4 was increased in tumor tissues and cell lines. Inhibition of miR-21, CXCR4, and miR-21 and CXCR4 together all reduced the migration, invasiveness, proliferation, and enhanced apoptosis in glioma cells, as well as reduced tumor volume and mass in xenograft model. The inhibition effect was strongest in double-targeted knockdown of miR-21 and CXCR4 group, whose downstream pathways involved in AKT axis and ERK axis activation. In conclusion, our findings reported that double-targeted knockdown of miR-21 and CXCR4 could more effectively inhibit the proliferation, migration, invasion, and growth of transplanted tumor and promote cell apoptosis, which were involved in the PI3K/AKT and Raf/MEK/ERK signaling pathways.
Highlights
Glioma is the most common and feared type of tumor, with an annual incidence of 1 per 10,000 population [1]
Evidence shows that miR-21 is overexpressed in gliomas and glioma cells compared to normal tissues, and its expression level is positively correlated with glioma grade [5, 6]
Numerous studies suggest that the overexpression of CXCR4 facilitates proliferation, angiogenesis, invasion, and metastasis, as well as chemotherapy and radiotherapy resistance of BioMed Research International glioma in several glioma cell lines and mouse models [16,17,18,19,20,21]
Summary
Glioma is the most common and feared type of tumor, with an annual incidence of 1 per 10,000 population [1]. Downregulation of miR-21 leads to repression of antiapoptotic capacity, reduction of migratory, and invasion, as well as increase of chemical-induced death in glioma cells [8, 11,12,13] All of these make miR-21 a potential glioma marker for diagnosis and prognosis but a target for novel therapeutic intervention. Numerous studies suggest that the overexpression of CXCR4 facilitates proliferation, angiogenesis, invasion, and metastasis, as well as chemotherapy and radiotherapy resistance of BioMed Research International glioma in several glioma cell lines and mouse models [16,17,18,19,20,21]. This study might pave ways for further research on glioma pathology and physiology
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