Nrf3 Promotes 5-FU Resistance in Colorectal Cancer Cells via the NF-κB/BCL-2 Signaling Pathway In Vitro and In Vivo

Figure 5

Nrf3 activates the NF-κB/BCL-2 signaling pathway. (a) The expression of Nrf3, RELA, P-RELA, and BCL-2. Overexpressed Nrf3 increased the expression of RELA, P-RELA, and BCL-2 in HT29. Knockdown of Nrf3 decreased the expression of RELA, P-RELA, and BCL-2 in SW620. (b) The typical graph of cell apoptosis. (c) The percentage of apoptosis after 5-FU and CAPE treatment (HT29 and HT29/Nrf3). (d) The percentage of apoptosis after 5-FU and TNFα treatment (SW620 and SW620/shNrf3). (e) The expression of Nrf3, RELA, P-RELA, and BCL-2 after 5-FU and CAPE addition (HT29 and HT29/Nrf3). (f) The expression of Nrf3, RELA, P-RELA, and BCL-2 after 5-FU and TNFα addition (SW620 and SW620/shNRF3). These results showed that the NF-κB/BCL-2 signaling pathway regulated Nrf3-mediated, 5-FU-induced cell apoptosis. Inhibition of the NF-κB/BCL-2 signaling pathway increased the 5-FU-induced cell apoptosis rate, and the activation of the NF-κB/BCL-2 signaling pathway decreased 5-FU-induced cell apoptosis.

(a)

(b)

(c)

(d)

(e)

(f)