Dicer induced reactive oxygen species inhibit hepatocellular carcinoma through interacting with cytochrome c oxidase

Figures & data

Figure 1. Dicer promoted the generation of ROS. (A) Identification of Dicer expression in pCMV-control and pCMV-Dicer transfected SMMC-7721 cells. (B) The COX activity of pCMV-Dicer cells was repressed compared with those of blank control or pCMV-control cells, *p < .05. (C) The ROS level of pCMV-Dicer cells was increased compared with those of blank control or pCMV-control.**p < .01.

Table 1. The ROS levels were positively associated with Dicer expression at borderline statistical level by chi-test analysis in HCC tissue.

Dicer	ROS		p-value
	High	Low
High	17	12	.065
Low	2	8

Figure 2. The influence of ADDA-5 hydrochloride or NAC treatment on COX activity and ROS production, respectively. (A) The COX activity of Dicer overexpressing cells was decreased after ADDA-5 hydrochloride intervention, **p < .01. (B) The ROS level of Dicer overexpressing cells was increased after ADDA-5 hydrochloride intervention, **p < .01. (C) The COX activity of Dicer overexpressing cells was decreased after NAC intervention, **p < .01. (D) The ROS level of Dicer overexpressing cells was decreased after NAC intervention, **p < .01.

Figure 3. Elevated ROS level promoted cell apoptosis, inhibited cell proliferation and migration of HCC cells in all groups of pCMV-Dicer or pCMV-control transfected cells and blank control. (A) H₂O₂ treatment elevated the cell apoptotic rate. *p < .05, vs. pCMV-control transfected cells; #p < .05 vs. cells without H₂O₂ intervention. (B) H₂O₂ treatment suppressed cell migration. *p < .05, vs. pCMV-control transfected cells; #p < .05 vs. cells without H₂O₂ intervention. (C) H₂O₂ treatment suppressed cell viability. *p < .05, vs. pCMV-control transfected cells; #p < .05 vs. cells without H₂O₂ intervention.

Data availability statement

The data supporting the findings of this study are available from the corresponding author upon reasonable request.