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Additional file 2: Figure S2. CircPTK2 promoted aggressive phenotypes of CRC cells in vitro. Cells were transfected with circPTK2 siRNA or circPTK2-overexpressing plasmid for 48 h. Then cells were harvested for annexin-V and PI staining. Cell apoptosis was detected with flow cytometry analysis. The cells were stained by crystal violet to evaluate cell proliferation, migration, and invasion capability. (A, B) The effect of circPTK2 knockdown on SW480 apoptosis. (C, D) The effect of circPTK2 overexpression on SW620 apoptosis. (E-H) Representative images and quantification results of the colony formation of cells. (I-L) Representative images and quantification results of the migration and invasion of cells. The data are the mean ± SEM. *P

Additional file 7: Table S1. Demographic information of colorectal cancer (CRC) and healthy control for PCR analysis.

Additional file 3: Figure S3. CircPTK2 promoted tumor growth in a xenograft mouse model. LOVO cells stably expressing luciferase were transfected with the indicated siRNAs and HCT15 cells stably expressing luciferase were transfected with the indicated overexpressing-plasmid. After 72 h, cells were injected into the tail veins of nude mice (n = 6). (A) Representative bioluminescence images of mice bearing LOVO cells were obtained. (B) Luciferase activity of tumor, liver, and lung was quantified in mice bearing LOVO cells. (C) Representative bioluminescence images of mice bearing HCT15 cells were obtained. (D) Luciferase activity of tumor, liver and lung was quantified in mice bearing HCT15 cells. The data are the mean ± SEM. *P

Additional file 9: Table S3. The detailed information of patients subjected to circRNA microarray analysis.

Additional file 1: Figure S1. The circPTK2 is elevated in serum of CRC patients. (A) Levels of circPTK2 in serum from healthy controls (NOR) and CRC patients (CRC) in the testing, validation, and the combination set were detected by qPCR. (B) The abundance of circPTK2 in CRC patients with different clinical characteristics were further analyzed. Data are presented as -ΔΔCt by one-way ANOVA with three technical replicates each. (C) Receiver operating characteristic (ROC) analysis was used to evaluate the diagnosis value of circPTK2 in CRC with different clinical characteristics. T: primary tumor; N: node metastasis; M: distant metastasis. Shown are the calculated ROC curves.

Additional file 10. Supplementary methods.

Additional file 4: Figure S4. The mass spectrometry of vimentin. Each mass spectrum represents a peptide. The protein binding to circPTK2 was vimentin.

Additional file 8: Table S2. Demographic information of colorectal cancer (CRC) patients subjected to TMA.

Additional file 6: Figure S6. CircPTK2 promoted MMP2/9 and CXCR4 expression in CRC cells. SW480 and HCT15 cells were transfected with circPTK2-overexpressing plasmid for 48 h, western blot assay showing circPTK2 overexpression up-regulated MMP2/9 and CXCR4.

Additional file 5: Figure S5. CircPTK2 targeted vimentin protein to regulate growth and metastasis of CRC. (A-B) HCT15 cells were transfected with circPTK2-overexpressing plasmid as well as vimentin siRNA for 48 h. Cells were used for staining with crystal violet or injected into subcutaneous tissue of nude mice. Colony formation and tumor growth were detected. Colony formation and tumor growth of HCT15 cells were shown. (C-D) LOVO cells were transfected with circPTK2 siRNA plasmid as well as vimentin-overexpressing plasmid for 48 h. Cells were used for staining with crystal violet or injected into subcutaneous tissue of nude mice. Colony formation and tumor growth of LOVO cells were shown. P values were calculated by t test.