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. 2022 Mar 1;23(5):2732. doi: 10.3390/ijms23052732

Figure 3.

Figure 3

ARMC4 functions as a negative regulator of NF-κB. (A) Western blot, showing that Flag-tagged ARMC4 was overexpressed in CRC cell lines HT29, DLD1, and HCT116 and HEK293 cells with the vector as the control (Ctrl) (left panel) and shARMC4 stable lines were also established with the sh-scramble (sh-scr) lines as the control (right panel). (B) NF-κB luciferase assay, showing ARMC4 overexpression cells exhibited decreased NF-κB activity compared to the Ctrl cells while the shARMC4 exhibited increased NF-κB activity compared to the sh-scr. (C) Assays of conditioned media, showing that conditioned media from HT29, DLD1, and HCT116 cells overexpressing ARMC4 had much lower NF-κB activation ability than vector ctrl cells. In contrast, conditioned media from shARMC4 knockdown cells in HT29, DLD1, and HCT116 cell lines had much higher NF-κB activation ability than sh-scr cells. Stable 293-NF-κB reporter cells were used to examine the media’s NF-κB activation ability. The data were normalized to the total number of cells that generated the conditioned media and to the total amounts of protein. The data represent the means ± SD from three independent experiments. * p < 0.05 ARMC4 vs. Ctrl group; # p < 0.05 shARMC4 vs. sh-scr group. * p < 0.05 Ctrl vs. ARMC4 group; # p < 0.05 sh-scr vs. shARMC4 group; n = 3.