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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: CircSCAP interacts with SF3A3 to inhibit the malignance of non-small cell lung cancer by activating p53 signaling

Fig. 1

CircSCAP is down-regulated and associated with poor prognosis in lung cancer. A Heatmap of differentially expressed circRNAs in three pairs of human lung cancer and adjacent non-tumor tissues. The red arrow indicated the circRNA of circSCAP. B Schematic of circSCAP biogenesis. CircSCAP was derived from the back-splicing of the linear transcript of SCAP (the host gene). The circularization site of circSCAP was validated via PCR and sanger sequencing. C Northern blot analysis of circSCAP transcript level in lung cancer tissues (upper). Relative expression level of circSCAP in 161 paired normal and lung cancer tissues, as detected by RT-PCR (lower). T, tumor; NAT: normal adjacent tissue. D The existence of circSCAP was validated by PCR using divergent and convergent primers for cDNA and gDNA of lung cancer cell lines. E Northern blot analysis indicated that circSCAP was resistant to RNase R digestion. F CircSCAP was located in the cytoplasm of A549 (left) and H1650 (right) lung cancer cells, as shown by subcellular fractionation. G Representative images of circSCAP subcellular location in H1650 (upper) and A549 cell line (lower), as displayed by fluorescence in situ hybridization (FISH). H The expression level of circSCAP in lung cancer tissues of stage T1 + T2 was higher than that of stage T3 + T4, and the difference was statistically significant (left). No significant difference was observed between the level of circSCAP and other clinical stages (middle and right). I Receiver operating characteristic (ROC) curve displayed the discrimination of overall survival in lung cancer patients using circSCAP expression level. J Lung cancer patients with the higher level of circSCAP showed the better prognosis. Data represent the mean ± SD of triplicate experiments and were analyzed by Student t test. * means P < 0.05

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