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Fig. 6 | Molecular Cancer

Fig. 6

From: hsa_circ_0007919 induces LIG1 transcription by binding to FOXA1/TET1 to enhance the DNA damage response and promote gemcitabine resistance in pancreatic ductal adenocarcinoma

Fig. 6

hsa_circ_0007919 binds FOXA1 and TET1 in GEM-resistant PDAC cells

(A) FISH analysis of the cellular localization of hsa_circ_0007919. The hsa_circ_0007919 probes were red while nuclei were stained with DAPI (1000×). (B) Nuclear-cytoplasmic fractionation assay analysis of hsa_circ_0007919 location in GEM-resistant PDAC cells, the U6 and GAPDH were used as nuclear and cytoplasmic controls. (C) Venn diagram showing overlapped genes between interacting with hsa_circ_0007919 and interacting with LIG1 promoter region. (D) Protein-protein interaction network analysis of proteins interact with FOXA1. (E-H) Expression of LIG1 in GEM-resistant PDAC cells with or without FOXA1 or TET1 inhibition. (I-J) IP assay analysis of the interaction between FOXA1 and TET1 in GEM-resistant PDAC cells. (K-L) Expression of LIG1 in FOXA1-silenced GEM-resistant PDAC cells with TET1 inhibition or overexpression. (M-N) ChIRP assay analysis of the interaction between hsa_circ_0007919 and FOXA1 or TET1 in GEM-resistant PDAC cells. (O-P) RIP assay analysis of the interaction between FOXA1 or TET1 and hsa_circ_0007919 in normal or GEM-resistant PDAC cells. Data are the means ± SDs (n = 3 independent experiments), ** p < 0.01, *** p < 0.001

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Molecular Cancer

ISSN: 1476-4598