ArticleBreast cancer research : BCR2013
Lapatinib-induced NF-kappaB activation sensitizes triple-negative breast cancer cells to proteasome inhibitors.
Article in Breast cancer research : BCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Artificial intelligence for precision oncology from phenotyping and drug discovery to clinical translation.Discover oncology · 2026Review
- IFI16 Induced by p53 Activates the NF-κB Pathway to Counteract Cisplatin-Induced Apoptosis in Cervical Cancer Cells.Journal of cellular and molecular medicine · 2025Article
- Promoter Hyper-methylation of ZNF662 Restrains its Tumor Suppressing Function in Triple-Negative Breast Cancer Through Regulating NGF Signaling Axis.International journal of biological sciences · 2025Article
- Disrupting DDB2-DNA Interaction by Lapatinib Enhances Chemotherapy Sensitivity.International journal of biological sciences · 2025Article
- Article
- Treatment Strategies Against Triple-Negative Breast Cancer: An Updated Review.Breast cancer (Dove Medical Press) · 2022Review
- miR-221 confers lapatinib resistance by negatively regulating p27Cancer science · 2021Article
- Emerging Biomarkers and Targeted Therapies in Feline Mammary Carcinoma.Veterinary sciences · 2021Review
- Curcumin: Modulator of Key Molecular Signaling Pathways in Hormone-Independent Breast Cancer.Cancers · 2021Review
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- RANK signaling increases after anti-HER2 therapy contributing to the emergence of resistance in HER2-positive breast cancer.Breast cancer research : BCR · 2021Article
- Tyrosine Kinase Inhibitors Are Promising Therapeutic Tools for Cats with HER2-Positive Mammary Carcinoma.Pharmaceutics · 2021Article
- The Role of the RANKL/RANK Axis in the Prevention and Treatment of Breast Cancer with Immune Checkpoint Inhibitors and Anti-RANKL.International journal of molecular sciences · 2020Review
- RelB sustains endocrine resistant malignancy: an insight of noncanonical NF-κB pathway into breast Cancer progression.Cell communication and signaling : CCS · 2020Article
- Identification of synergistic drug combinations using breast cancer patient-derived xenografts.Scientific reports · 2020Article
- Screening and Identification of Key Biomarkers in Acquired Lapatinib-Resistant Breast Cancer.Frontiers in pharmacology · 2020Article
- Tumor Necrosis Factor α Blockade: An Opportunity to Tackle Breast Cancer.Frontiers in oncology · 2020Review
- Combining RANK/RANKL and ERBB-2 targeting as a novel strategy in ERBB-2-positive breast carcinomas.Breast cancer research : BCR · 2019Article
- Proteostasis In The Endoplasmic Reticulum: Road to Cure.Cancers · 2019Review
- A phase I study of HER1, HER2 dual kinase inhibitor lapatinib plus the proteasome inhibitor bortezomib in patients with advanced malignancies.Cancer chemotherapy and pharmacology · 2019Article
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTriple-negative breast cancer (TNBC), a subtype of breast cancer with negative expressions of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (HER2), is frequently diagnosed in younger women and has poor prognosis for disease-free and overall survival. Due to the lack of known oncogenic drivers for TNBC proliferation, clinical benefit from currently available targeted therapies is limited, and new therapeutic strategies are urgently needed.
methodsTriple-negative breast cancer cell lines were treated with proteasome inhibitors in combination with lapatinib (a dual epidermal growth factor receptor (EGFR)/HER2 tyrosine kinase inhibitor). Their in vitro and in vivo viability was examined by MTT assay, clonogenic analysis, and orthotopic xenograft mice model. Luciferase reporter gene, immunoblot, and RT-qPCR, immunoprecipitation assays were used to investigate the molecular mechanisms of action.
resultsOur data showed that nuclear factor (NF)-κB activation was elicited by lapatinib, independent of EGFR/HER2 inhibition, in TNBCs. Lapatinib-induced constitutive activation of NF-κB involved Src family kinase (SFK)-dependent p65 and IκBα phosphorylations, and rendered these cells more vulnerable to NF-κB inhibition by p65 small hairpin RNA. Lapatinib but not other EGFR inhibitors synergized the anti-tumor activity of proteasome inhibitors both in vitro and in vivo. Our results suggest that treatment of TNBCs with lapatinib may enhance their oncogene addiction to NF-κB, and thus augment the anti-tumor activity of proteasome inhibitors.
conclusionsThese findings suggest that combination therapy of a proteasome inhibitor with lapatinib may benefit TNBC patients.
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