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. 2022 May 4;13(5):433. doi: 10.1038/s41419-022-04805-w

Fig. 6. SP1 facilitates the tumorigenesis of CRC cells in vivo by regulating theTUG1/miR-421/KDM2A/ERK axis.

Fig. 6

A Western blot assay for p-ERK and ERK protein levels in HCT116 and SW480 cells transfected with si-KDM2A. B Western blot assay for KDM2A, p-ERK and ERK protein levels in HCT116 and SW480 cells transfected with miR-421 inhibitor, si-KDM2A or both. C Western blot assay for KDM2A, p-ERK, and ERK protein levels in HCT116 and SW480 cells transfected with si-TUG1-1, miR-421 inhibitor, or both. D Tumor volume in nude mice treated with sh-SP1 or combined with oe-KDM2A at different time points. E RT-qPCR determination of SP1, TUG1, miR-421, and KDM2A expression in the tumor tissues of mice treated with sh-SP1 or combined with oe-KDM2A. F Immunohistochemical staining of KDM2A protein in tumor tissues of mice treated with sh-SP1 or combined with oe-KDM2A. G Western blot assay of KDM2A, p-ERK, and ERK expression in tumor tissues of mice treated with sh-SP1 or combined with oe-KDM2A. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001, compared with HCT116 and SW480 cells transfected with si-NC or inhibitor NC + si-NC, or mice treated with sh-NC. #p < 0.05, ##p < 0.01, ###p < 0.001, and ####p < 0.0001, compared with HCT116 and SW480 cells transfected with miR-421 inhibitor + si-NC or si-TUG1-1 + inhibitor NC, or mice treated with sh-SP1 + oe-NC. The measurement data are expressed as mean ± standard deviation. Comparison between two groups was conducted by unpaired t-test. Multi-group comparison at different time points was performed using two-way ANOVA, followed by Bonferroni post hoc test, n = 12.