ArticleCancer biology & therapy2019
Dual-target MDM2/MDMX inhibitor increases the sensitization of doxorubicin and inhibits migration and invasion abilities of triple-negative breast cancer cells through activation of TAB1/TAK1/p38 MAPK pathway.
Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Murine double minute 2 (MDM2) as an appealing target for natural products in cancer treatment.Molecular biology reports · 2026Review
- Proteomics on choroidal neovascularization based on itraq and the protective effect of TAB1 in CNV.Scientific reports · 2025Article
- Pharmacological Inhibition of MDM2 Induces Apoptosis in p53-Mutated Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
- Article
- Targeting MDM2-p53 interaction for breast cancer therapy.Oncology research · 2025Review
- MDM2: current research status and prospects of tumor treatment.Cancer cell international · 2024Review
- MDMX in Cancer: A Partner of p53 and a p53-Independent Effector.Biologics : targets & therapy · 2024Review
- MDM2- an indispensable player in tumorigenesis.Molecular biology reports · 2023Review
- Association between TP53 mutation and high 21-gene recurrence score in estrogen receptor-positive/HER2-negative breast cancer.NPJ breast cancer · 2022Article
- Application of Microfluidic Systems for Breast Cancer Research.Micromachines · 2022Review
- Therapeutic opportunities in cancer therapy: targeting the p53-MDM2/MDMX interactions.American journal of cancer research · 2021Review
- A novel prognostic two-gene signature for triple negative breast cancer.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Elevated estrogen receptor β expression in triple negative breast cancer cells is associated with sensitivity to doxorubicin by inhibiting the PI3K/AKT/mTOR signaling pathway.Experimental and therapeutic medicine · 2020Article
- LIMD1 Increases the Sensitivity of Lung Adenocarcinoma Cells to Cisplatin via the GADD45α/p38 MAPK Signaling Pathway.Frontiers in oncology · 2020Article
- Cellular Plasticity in Breast Cancer Progression and Therapy.Frontiers in molecular biosciences · 2020Review
- The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma.Molecular cancer · 2019Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) has a poor prognosis mainly due to insensitivity or resistance to standard anthracycline- and taxane-based chemotherapy, urgently calling for new adjuvants to reverse drug resistance. Dual-target murine double minute 2 (MDM2) and murine double minute X (MDMX) inhibitor has been proved to play a critical part against cancer, particularly focusing on the tremendous potential to enhance the efficacy of doxorubicin (DOX), however little was reported in TNBC. In the present study, we investigated the synergistic antitumor effect of the MDM2/MDMX inhibitor with DOX using three TNBC cell lines, two in situ transplantation tumor models and 214 clinical samples. We observed that the MDM2/MDMX inhibitor combined with DOX could not only inhibit cell vitality and migration and invasion abilities, but also highly inhibit tumor growth in TNBC nude mice. Besides, co-treatment of MDM2/MDMX inhibitor and DOX suppressed epithelial to mesenchymal transition (EMT) through increasing the TAK1-binding protein 1 (TAB1), transforming growth factor β-activated kinase 1 (TAK1) and p38 mitogen-activated protein kinase (MAPK) expression. Small interfering RNA-mediated TAB1 knockdown induced the EMT, desensitized cells to DOX and enhanced the migration and invasion abilities. High MDM2/MDMX expression was positively associated with weak TAB1 expression in 214 TNBC tumor tissues confirmed by immumohistochemical staining and MDM2/MDMX/TAB1 expression was significantly related to TNBC patient survival. These findings indicate that dual-target MDM2/MDMX inhibitor could increase the sensitization of doxorubicin and inhibit migration and invasion abilities in TNBC cells through p38 MAPK pathway activation caused EMT suppression and hence could be useful in TNBC treatments in future.
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