ArticleOncology letters2022
NRBP1 negatively regulates SALL4 to reduce the invasion and migration, promote apoptosis and increase the sensitivity to chemotherapy drugs of breast cancer cells.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- SALL4-targeted therapeutic peptide PEN-FFW suppresses PD-L1 and enhances CD8⁺ T cell cytotoxicity via regulating PI3K/AKT signaling in breast cancer.Immunologic research · 2026Article
- TRIM24 promotes proliferation and metastasis of gastric cancer via mediating NRBP1 ubiquitination.Cell death & disease · 2025Article
- Integrative multi-omics analysis of druggable genes for therapeutic target identification in polycystic ovary syndrome.Journal of ovarian research · 2025Article
- Mutation characteristics and molecular evolution of ovarian metastasis from gastric cancer and potential biomarkers for paclitaxel treatment.Nature communications · 2024Article
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- Role of SALL4 in HER2+ Breast Cancer Progression: Regulating PI3K/AKT Pathway.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
The incidence of breast cancer (BC) ranks first among all kinds of female malignancies. Its invasion, migration, apoptosis and resistance to chemotherapeutic drugs are the focus of current research. Nuclear receptor binding protein 1 (NRBP1) and spalt-like transcription factor 4 (SALL4), which are observed to be abnormally expressed in BC, are investigated herein to identify their involvement in invasion, migration, apoptosis and chemotherapeutic drug sensitivity of BC and to elucidate the underlying mechanism. After NRBP1 was overexpressed by cell transfection, wound healing and Transwell experiments were used to detect the abilities of cell invasion and migration, and western blotting was used to detect the expression of MMP2 and MMP9. Cell viability and apoptosis were detected by Cell Counting Kit-8 assay, TUNEL staining and western blotting, in which Doxorubicin (DOX) and cis-platinum (Cis) were administrated after overexpression of NRBP1. Finally, after overexpression of NRBP1 and SALL4, the cell invasion, migration and apoptosis, and the sensitivity to DOX and Cis, were detected to explore the underlying mechanism. Overexpression of NRBP1 inhibited the invasion and migration, promoted the apoptosis, and enhanced the chemotherapeutic effect of chemotherapy drugs in BC cells. Overexpression of SALL4 in cells blocked the effects of NRBP1 overexpression on invasion, migration, apoptosis and DOX and Cis drug sensitivity of BC cells. In conclusion, NRBP1 negatively regulated SALL4 to reduce the invasion and migration capacities, promote apoptosis and increase the sensitivity to chemotherapeutic drugs of BC cells.
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