Skip to main content
. 2017 Sep 7;8(52):89451–89464. doi: 10.18632/oncotarget.20702

Figure 3. BMAL1 didn't function as an upstream factor of SP1-mediated DNMT1, DAB2IP and downstream pathway in JEG-3 cells.

Figure 3

A. The mRNA and protein abundance of DNMT1, MMP2 and MMP9 after DNMT1 knock-down in JEG-3 cells. The panel from left to right is the representative images of western blot assays, the immunoreactive bands densitometrically quantified and mRNA abundance. B. The mRNA and protein abundance of DAB2IP, MMP2 and MMP9 after DAB2IP knock-down in JEG-3 cells. C. The mRNA and protein abundance of SP1, DNMT1, DAB2IP, MMP2 and MMP9 after SP1 knock-down in JEG-3 cells. D. The mRNA and protein abundance of BMAL1, SP1, DNMT1, DAB2IP, MMP2 and MMP9 after BMAL1 knock-down in JEG-3 cells. β-Actin was used as a loading control. Blots are representative, and data are means ± SEM from three to four experiments.* P < 0.05, ** P < 0.01,*** P < 0.001 against si-NC cells.