Background Renal cell carcinoma (RCC) is a common lethal urological malignancy. Circular RNAs are assumed to play important roles in cancer development. The objective of the present study was to investigate the role and action mechanism of circ_0008717 in RCC. Methods The expression of circ_0008717, miR‐217 and F‐box protein 17 (FBXO17) mRNA was detected by a real‐time quantitative polymerase chain reaction. Cell proliferation was examined using a cell counting kit‐8 assay and an 5‐ethynyl‐2′‐deoxyuridine assay. Cell apoptosis was assessed by a flow cytometry assay. Cell migration and cell invasion were investigated using a transwell assay. Glycolysis progression was assessed according to the levels of glucose uptake and lactate production. The expression of glycolysis‐related proteins and FBXO17 protein was quantified by western blotting. The targets were analyzed by the bioinformatics tools (starBase and circinteractome) and validated by a dual‐luciferase reporter assay, RNA pull‐down assay and RNA immunoprecipitation assay. A xenograft model was established to monitor the role of circ_0008717 in vivo. Results Circ_0008717 was upregulated in RCC tissues and cells. Silencing circ_0008717 suppressed RCC cell proliferation, migration, invasion and glycolysis but promoted cell apoptosis. MiR‐217 was a target of circ_0008717 and bound to the FBXO17 3′ untranslated region. The expression of FBXO17 was positively regulated by circ_0008717 but impaired by miR‐217 reintroduction. The inhibitory effects of circ_0008717 knockdown on RCC cell malignant behaviors were reversed by miR‐217 inhibition or FBXO17 overexpression. Circ_0008717 knockdown inhibited tumor growth in vivo by regulating miR‐217 and FBXO17. Conclusions Circ_0008717 aggravated the progression of RCC by activating FBXO17 through targeting miR‐217, which provided a novel mechanism for circ_0008717 to participate in RCC progression.
Prostate carcinoma is a common malignant tumor of the male genitourinary system. Toosendanin can inhibit the biological behavior of a variety of malignant tumor cells (such as ovarian carcinoma, lung carcinoma, and breast carcinoma, etc.), but its effect on the malignant behavior of prostate carcinoma cells and its mechanism are not yet understood. Therefore, this article discusses the influence of toosendanin on the multiplication, apoptosis, migration, and invasion of prostate carcinoma cells and its possible mechanism. Different doses (0.125, 0.25, 0.5 ^M) of toosendanin can reduce the cell viability, number of colonies, number of migrating cells, number of invasive cells, and Bcl-2 protein and FOXC2-AS1 levels of prostate carcinoma cells, as well as increase the apoptosis rate and Bax protein level. Overexpression of FOXC2-AS1 can increase the cell viability, number of colonies formed, number of migrating cells, number of invasive cells, and Bcl-2 protein expression, as well as reduce the rate of apoptosis and Bax protein level after toosendanin treatment of prostate carcinoma cells. It was demonstrated that toosendanin may inhibit the multiplication, migration, and invasion of prostate carcinoma cells and promote its apoptosis by down-regulating FOXC2-AS1 expression.
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