C1orf63 silencing affects breast cancer cell proliferation, apoptosis, and cycle distribution by NF-κB signaling pathway.

OBJECTIVE To investigate the effect of C1orf63 on breast cancer cell (BCC) proliferation, apoptosis, and cycle distribution and related mechanisms. METHODS The expression of C1orf63 was interfered with in BCC line MCF and cells were divided into a C1orf63 overexpression group, C1orf63 silence group, blank group, and empty group. The mRNA expression of C1orf63 and the proliferation, apoptosis, and cycle distribution of BCCs were detected. The mRNA expression levels of NF-κB signaling pathway factors (p-IκBα, CyclinD1, CDK4, Bcl-2, and Bax) in each group were also detected. RESULTS There was no significant difference between the blank group and empty group in the expression level of C1orf63 mRNA, cell proliferation rate, apoptosis rate, cell distribution rate, or mRNA expression levels of the NF-κB signaling pathway factors (all P>0.05). The expression levels of C1orf63 mRNA in the C1orf63 silenced group were lower than those in the other two groups (P<0.05). The cell proliferation rate, cell distribution in S phase and G2/M phase, and the mRNA expression levels of NF-κB signaling pathway factors (p-IκBα, CyclinD1, CDK4, and Bcl-2) in the C1orf63 silenced group at each time point were lower than those in the other two groups (all P<0.05). The apoptosis rate, cells in G1 phase, and the Bax mRNA expression level in C1orf63 silenced group at each time point were higher than those in the other two groups (all P<0.05). CONCLUSION Down-regulation of C1orf63 acts on the NF-κB signaling pathway to regulate the expression of p-IκBα, CyclinD1, and CDK4, so as to inhibit BCC proliferation, promote cell apoptosis, and block the cell cycle.