Our study aimed to explore the involvement of circ_0001583 in the progression of glioblastoma (GBM). The expression levels of CircRNA in GBM were examined using the GEO database, and quantification of circ_0001583 levels was performed through qRT-PCR in both GBM tissues and cell lines. Survival analysis was conducted using Kaplan-Meier plots. The effects of circ_0001583 knockdown on cell proliferation, invasion, and glycolysis were evaluated through functional assays and measurements of glycolytic activity. Bioinformatics and reporter assays revealed that miR-647 serves as a target for circ_0001583. Tumorigenesis following circ_0001583 knockdown was investigated in a nude mouse model utilizing U251 cells. Additionally, a co-culture system with normal human astrocytes (NHAs) and GBM-conditioned medium was employed to study circ_0001583 expression and its influence on cell proliferation. The presence of circ_0001583 in normal human astrocytes was assessed using PKH67 labeling and immunofluorescence techniques. Bioinformatics analyses revealed a notable increase in the expression of circ_0001583 in GBM, correlating with metastasis. The inhibition of circ_0001583 expression led to decreased viability, proliferation, and invasive potential of GBM cells. It was found that circ_0001583 targets miR-647, which is downregulated in GBM. Silencing circ_0001583 resulted in elevated levels of miR-647. CKAP2L, a target of miR-647, showed an overexpression in GBM cases. Additionally, a positive relationship was established between circ_0001583 and CKAP2L, contrasting with a negative association with miR-647. An increase in miR-647 expression led to a decrease in CKAP2L protein levels. Rescue assays further validated that circ_0001583 influences the functions of GBM cells through the miR-647/CKAP2L pathway. In vivo investigations demonstrated that the knockdown of circ_0001583 resulted in retarded tumor growth, enhanced levels of miR-647, and diminished expression of Ki-67, CKAP2L, HK2, and LDHA within tumors. Moreover, co-culture studies involving GBM-conditioned medium demonstrated an upregulation of circ_0001583 in NHAs, which promoted cell proliferation. Our data collectively suggest that exosomal circ_0001583 promotes glioblastoma progression via the miR-647/CKAP2L pathway.