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.

Download full-text PDF

Source
http://dx.doi.org/10.14715/cmb/2022.68.4.17DOI Listing

Publication Analysis

Top Keywords

breast cancer
28
cancer cells
20
xenograft tumor
12
tumor model
12
model mice
12
treated sfn
12
gene expression
12
sfn
11
bioactive compound
8
cancer
8

Similar Publications

CXCR4 promotes tumor stemness maintenance and CDK4/6 inhibitors resistance in ER-positive breast cancer.

Breast Cancer Res

January 2025

Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.

Background: CDK4/6 inhibitors have significantly improved the survival of patients with HR-positive/HER2-negative breast cancer, becoming a first-line treatment option. However, the development of resistance to these inhibitors is inevitable. To address this challenge, novel strategies are required to overcome resistance, necessitating a deeper understanding of its mechanisms.

View Article and Find Full Text PDF

Background: Patients who actively engage in their medical decision-making processes can experience better health outcomes. This exploratory study aimed to identify predictors of preferred and actual roles in decision-making in healthy women with BRCA1/2 pathogenic variants (PVs).

Methods: Women with BRCA1/2 PVs without a history of breast and/or ovarian cancer were recruited in six centres across Germany.

View Article and Find Full Text PDF

Targeting MYC for the treatment of breast cancer: use of the novel MYC-GSPT1 degrader, GT19630.

Invest New Drugs

January 2025

UCD School of Medicine, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland.

Background: Since MYC is one of the most frequently altered driver genes involved in cancer formation, it is a potential target for new anti-cancer therapies. Historically, however, MYC has proved difficult to target due to the absence of a suitable crevice for binding potential low molecular weight drugs.

Objective: The aim of this study was to evaluate a novel molecular glue, dubbed GT19630, which degrades both MYC and GSPT1, for the treatment of breast cancer.

View Article and Find Full Text PDF

Purpose: Build machine learning (ML) models able to predict pathological complete response (pCR) after neoadjuvant chemotherapy (NAC) in breast cancer (BC) patients based on conventional and radiomic signatures extracted from baseline [F]FDG PET/CT.

Material And Methods: Primary tumor and the most significant lymph node metastasis were manually segmented in baseline [F]FDG PET/CT of 52 newly diagnosed BC patients. Clinical parameters, NAC and conventional semiquantitative PET parameters were collected.

View Article and Find Full Text PDF

Micropeptide hSPAR regulates glutamine levels and suppresses mammary tumor growth via a TRIM21-P27KIP1-mTOR axis.

EMBO J

January 2025

Department of Geriatrics, Gerontology Institute of Anhui Province, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.

mTOR plays a pivotal role in cancer growth control upon amino acid response. Recently, CDK inhibitor P27KIP1 has been reported as a noncanonical inhibitor of mTOR signaling in MEFs, via unclear mechanisms. Here, we find that P27KIP1 degradation via E3 ligase TRIM21 is inhibited by human micropeptide hSPAR through its C-terminus (hSPAR-C), causing P27KIP1's cytoplasmic accumulation in breast cancer cells.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!