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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Extracellular vesicle-packaged circBIRC6 from cancer-associated fibroblasts induce platinum resistance via SUMOylation modulation in pancreatic cancer

Fig. 1

Correlation of circBIRC6 with response to oxaliplatin-based chemotherapy. (A) Graphical representation of the process used to identify elevated levels of circBIRC6 in CAFs from oxaliplatin-resistant patients. (B) qRT-PCR analysis of 10 selected circRNAs in both NAFs and CAFs (n = 3). (C) Comparative analysis of circBIRC6 expression in CAFs obtained from oxaliplatin-resistant (OXA-R) and -sensitive (OXA-S) pancreatic cancer patients via qRT–PCR (n = 3). (D) qRT-PCR evaluation of circBIRC6 expression in OXA-S (n = 31) and OXA-R (n = 51) PDAC samples, depicted as violin plots. (E-F) Kaplan–Meier survival analysis for advanced PDAC patients receiving oxaliplatin-based (E) or non-platinum chemotherapy (F), stratified by high or low circBIRC6 expression. (G) Genomic loci diagram depicting the exonic origin (exons 2 to 10) of circBIRC6. (H) Validation of the back-splice junction of circBIRC6 using Sanger sequencing. (I) Amplification of cDNA and gDNA in CAFs using convergent and divergent primers, with GAPDH as a negative control. (J) Temporal analysis of circBIRC6 and BIRC6 mRNA expression in CAFS post-treatment with actinomycin D. (K) Comparative PCR analysis of circBIRC6, BIRC6, and GAPDH expression in CAFs following RNase R treatment. Data are mean ± SD. n.s., not significant. *p < 0.05, **p < 0.01, ***p < 0.001

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