CircASXL1 knockdown represses the progression of colorectal cancer by downregulating GRIK3 expression by sponging miR-1205
CircASXL1 knockdown represses the progression of colorectal cancer by downregulating GRIK3 expression by sponging miR-1205
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Abstract Background Colorectal cancer Furniture Set (CRC) is a common aggressive tumor that poses a heavy burden to human health.An increasing number of studies have reported that circular RNA (circRNA) is involved in the progression of CRC.In this study, the special profiles of circASXL1 (circ_0001136) in CRC progression were revealed.
Methods The expression of circASXL1, microRNA-1205 (miR-1205), and glutamate ionotropic receptor kainate type subunit 3 (GRIK3) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR).The protein expression was determined by Western blot or immunohistochemistry.Cell colony-forming ability was investigated by colony formation assay.
Cell cycle and apoptosis were demonstrated using cell-cycle and cell-apoptosis analysis assays, respectively.Cell migration and invasion were detected by wound-healing and transwell migration and invasion assays, respectively.The binding sites between miR-1205 and circASXL1 or GRIK3 were predicted by circBank or miRDB online database, and identified by dual-luciferase reporter assay.
The impact of circASXL1 on tumor formation in vivo was investigated by in vivo tumor formation assay.Results CircASXL1 and GRIK3 expression were apparently upregulated, and miR-1205 expression was downregulated in CRC tissues and cells relative to control groups.CircASXL1 knockdown inhibited cell colony-forming ability, migration and invasion, whereas induced cell arrest at G0/G1 phase and cell apoptosis in Wheelchair Accessories CRC cells; however, these effects were attenuated by miR-1205 inhibitor.
Additionally, circASXL1 acted as a sponge for miR-1205, and miR-1205 was associated with GRIK3.Furthermore, circASXL1 silencing hindered tumor formation by upregulating miR-1205 and downregulating GRIK3 expression.Conclusion CircASXL1 acted an oncogenic role in CRC malignant progression via inducing GRIK3 through sponging miR-1205.
Our findings provide a theoretical basis for studying circASXL1-directed therapy for CRC.