Cauliflower bioactive compound sulforaphane inhibits breast cancer development by suppressing NF-κB /MMP-9 signaling pathway expression.

In recent years, anti-cancer plant food development and research have received increasing attention, and cauliflower is one of the vegetables with anti-cancer effects. Sulforaphane (SFN) is one of the main anti-cancer components in cauliflower. In this study, the mechanism of action of SFN in anti-breast cancer was investigated using SFN, a bioactive compound extracted from cauliflower. For this purpose, SFN was extracted from cauliflower using rotary evaporation and silica gel chromatography, and the extracted SFN was used for in vitro and in vivo experiments. Breast cancer cells MCF-7, MDA-MB-231 and MDA-MB-231 xenograft tumor model mice were treated with SFN, pcDNA3.1-MMP-9, Si-RNA- MMP-9 and Si-RNA-NF-κB, respectively, and the corresponding saline treatment or blank plasmid treatment was used as control. The gene expression of NF-κB and MMP-9 in each group was detected by RT-PCR, and the protein phosphorylation level of MMP-9 was measured by Western bloting assay. WST 1 assay, MTT assay and flow cytometric analysis were used to detect the activity, proliferation and apoptosis levels of breast cancer cells. The tumor histopathology of the xenograft tumor model mice after SFN treatment was examined by HE staining. Results showed that Breast cancer cells treated with SFN showed reduced cell proliferation, decreased cell activity, increased apoptosis ratio, and inhibited gene expression and protein phosphorylation of MMP-9 as well as gene expression of NF-κB (P < 0.05). The same effect occurred with transfection of Si-RNA- MMP-9 and Si-RNA-NF-κB in breast cancer cells, while transfection of pcDNA3.1-MMP-9 plasmid significantly redeemed the inhibitory effect of SFN on breast cancer cells (P < 0.05). MDA-MB-231 xenograft tumor model mice treated with SFN showed significant improvement in the pathological condition of the tumor tissue. Then, SFN may inhibit breast cancer development by regulating the NF-κB /MMP-9 signaling pathway.

miR-190a-5p regulates cardiomyocytes response to ferroptosis via directly targeting GLS2.

Ferroptosis is a novel identified form of regulated cell death that has been implied in the pathology of myocardial infarction (MI). However, the regulation mechanisms of ferroptosis in cardiomyocyte are still elusive. MiRNAs are a group of small non-coding RNAs that play crucial roles in various biological activities. Till now, little is known about the role of miRNA in the ferroptosis of cardiomyocytes. In the current study, we found that miR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe 2+ accumulation. Meanwhile, inhibition of miR-190a-5p caused upregulation of GLS2, resulting in opposite effects which could be blocked by GLS2 inhibitor compound 968. In summary, our findings suggest that miR-190a-5p plays an essential role in regulation of ferroptosis of cardiomyocytes and suggest a potential therapeutic target for MI.