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. 2023 Jul 31;19(12):3970–3986. doi: 10.7150/ijbs.81895

Figure 4.

Figure 4

Niraparib inhibits the transcription of DIMT1 through promoting Pol II pausing in a PAR-dependent manner. (A) Genome browser tracks of PARP-1 ChIP-seq data and RNA-seq data around the DIMT1 gene in Cal-62 cells treated with DMSO and niraparib are shown. (B) ChIP-qPCR was performed with Cal-62 cells using PARP1 and IgG antibodies to determine the expression levels of DIMT1 in Cal-62 cells treated with DMSO and niraparib. The results were presented relative to the IgG samples. (C) The effect of DRB on the expression of DIMT1 induced by PARP1 overexpression as determined by qRT-PCR. (D-E) Cal-62 cells were lysed with RIPA buffer, and lysates were subjected to immunoprecipitation using either anti-IgG, anti-PARP1, or anti-NELF-E antibodies, and analyzed by western blot with indicated antibodies. (F) Cal-62 cells treated with niraparib or DMSO and lysates were subjected to immunoprecipitation using anti-NELF-E and analyzed by western blot with indicated antibodies. (G) Western blot of NELF-E in Cal-62 cells treated with DMSO and niraparib. (H) Cal-62 cells treated with niraparib or DMSO and lysates were subjected to immunoprecipitation using anti-NELF-E and analyzed by western blot with indicated antibodies. ChIP-qPCR was performed with Cal-62 cells using Pol II (I), phosphoS2 Pol II (J), and IgG antibodies to determine the expression levels of DIMT1 in Cal-62 cells treated with DMSO and niraparib. The results were presented relative to the IgG samples. The data are presented as the mean ± SD. All *p < 0.05, **p < 0.01, ***p < 0.001.