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. 2016 Aug 5;7(36):57866–57877. doi: 10.18632/oncotarget.11077

Figure 3. KDM4B plays an essential role in mitochondrial apoptosis.

Figure 3

(A and B) KDM4B knockdown led to a decrease in mitochondrial membrane potential in LoVo cells. The mitochondrial membrane was stained with JC-1, which exists as a green fluorescent monomer at low membrane potential and as red fluorescent aggregates at high membrane potential. The ratio of green to red fluorescence of JC-1 reflects the ratio of apoptosis. LoVo cells were treated with siControl (8.83 ± 1.47) or siKDM4B (1#, 47.28 ± 11.15) for 72 h, then mitochondrial membrane potential was tested by JC-1 staining analysis.(B, P < 0.01). (C and D) KDM4B knockdown led to a decrease in mitochondrial membrane potential in SW48 cells. SW48 cells were treated with siControl (14.60 ± 3.87) or siKDM4B (1#, 40.84 ± 7.52) for 72 h, then mitochondrial membrane potential was tested by JC-1 staining analysis.(D, P < 0.01) (E) Expression levels of BFAR, MLLT11, MSRB2, and HAX1 in LoVo cells following treatment with siKDM4B for 72 h. mRNA levels were analyzed by quantitative RT- PCR.(*P < 0.05; **P < 0.01) (F and G) Expression levels of HAX1 in colorectal cancer cells (LoVo, SW48, SW480, SW620) following treatment with siKDM4B for 72 h by quantitative RT-PCR (siKDM4B 1#) and western blot (siKDM4B 1, 2, 3#). (**P < 0.01; ***P < 0.001) All qRT-PCR data were normalized to 18s ribosomal RNA, and α-tubulin was used as a loading control for western blots.