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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: ITPR3 facilitates tumor growth, metastasis and stemness by inducing the NF-ĸB/CD44 pathway in urinary bladder carcinoma

Fig. 2

Significant overexpression of ITPR3 in bladder cancer is attributed to demethylation of its promoter. a The methylation status of ITPR3 in SV-HUC-1, 5637 and 253 J cells was analyzed by bisulfite sequencing PCR (BSP). The 43 CpG sites in 10 clones were represented. The solid circle represents the methylated cytosine, and the hollow circle represents the unmethylated cytosine. b Analysis of the linear correlation between the mRNA level and methylation level of ITPR3 based on TCGA data. c Predicted CpG islands in the promoter region of ITPR3. Numbers indicate the positions in bp relative to the transcription start site. The blue regions represent the CpG islands, and the red vertical bars are the CpG loci in these input sequences. The promoter methylation level (d) and mRNA expression level (e) of ITPR3 in bladder cancer and normal tissue were examined through the UALCAN website based on the TCGA dataset. f ITPR3 protein levels were detected by a western blot assay in SV-HUC-1 cells after treatment with different doses of 5-Aza (0 μM, 2.5 μM and 5 μM) for 72 h. β-actin was used as an internal loading control

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