ArticleOncotarget2015
Lapatinib increases motility of triple-negative breast cancer cells by decreasing miRNA-7 and inducing Raf-1/MAPK-dependent interleukin-6.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Phosphoproteomic analysis reveals the diversity of signaling behind ErbB-inhibitor-induced phenotypes.The FEBS journal · 2025Article
- Disrupting DDB2-DNA Interaction by Lapatinib Enhances Chemotherapy Sensitivity.International journal of biological sciences · 2025Article
- Article
- Article
- Recent Advances with Precision Medicine Treatment for Breast Cancer including Triple-Negative Sub-Type.Cancers · 2023Review
- Role of MicroRNA-7 (MiR-7) in Cancer Physiopathology.International journal of molecular sciences · 2022Review
- Triple-Negative Breast Cancer: A Brief Review About Epidemiology, Risk Factors, Signaling Pathways, Treatment and Role of Artificial Intelligence.Frontiers in molecular biosciences · 2022Review
- Circular RNA regulates the onset and progression of cancer through the mitogen-activated protein kinase signaling pathway.Oncology letters · 2021Review
- Precision Medicine and Triple-Negative Breast Cancer: Current Landscape and Future Directions.Cancers · 2021Review
- Article
- PKCδ-mediated SGLT1 upregulation confers the acquired resistance of NSCLC to EGFR TKIs.Oncogene · 2021Article
- Expression profiles of circular RNAs in colon biopsies from Crohn's disease patients by microarray analysis.Journal of clinical laboratory analysis · 2021Article
- Tweaking EMT and MDR dynamics to constrain triple-negative breast cancer invasiveness by EGFR and Wnt/β-catenin signaling regulation.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- The Role of miRNA-7 in the Biology of Cancer and Modulation of Drug Resistance.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Elevated microRNA-7 inhibits proliferation and tumor angiogenesis and promotes apoptosis of gastric cancer cells via repression of Raf-1.Cell cycle (Georgetown, Tex.) · 2020Article
- CircRNAs in anticancer drug resistance: recent advances and future potential.Molecular cancer · 2020Review
- Triple-Negative Breast Cancer: A Review of Conventional and Advanced Therapeutic Strategies.International journal of environmental research and public health · 2020Review
- Potential Regulatory Roles of MicroRNAs and Long Noncoding RNAs in Anticancer Therapies.Molecular therapy. Nucleic acids · 2018Review
- Precision medicine based on tumorigenic signaling pathways for triple-negative breast cancer.Oncology letters · 2018Review
- Advances in studies of tyrosine kinase inhibitors and their acquired resistance.Molecular cancer · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lapatinib, a dual epidermal growth factor receptor (EGFR) and HER2 tyrosine kinase inhibitor (TKI), has been approved for HER2-positive breast cancer patients. Nevertheless, its inhibitory effect on EGFR did not deliver clinical benefits for triple-negative breast cancer (TNBC) patients even EGFR overexpression was frequently found in this disease. Moreover, lapatinib was unexpectedly found to enhance metastasis of TNBC cells, but the underlying mechanisms are not fully understood. In this study, we explored that the level of interleukin-6 (IL-6) was elevated in lapatinib-treated TNBC cells. Treatment with IL-6 antibody abolished the lapatinib-induced migration. Mechanistically, the signaling axis of Raf-1/mitogen-activated protein kinases (MAPKs), c-Jun N-terminal kinases (JNKs), p38 MAPK, and activator protein 1 (AP-1) was activated in response to lapatinib treatment to induce IL-6 expression. Furthermore, our data showed that microRNA-7 directly binds and inhibits Raf-1 3'UTR activity, and that down-regulation of miR-7 by lapatinib contributes to the activation of Raf-1 signaling pathway and the induction of IL-6 expression. Our results not only revealed IL-6 as a key regulator of lapatinib-induced metastasis, but also explored the requirement of miR7/Raf-1/MAPK/AP-1 axis in lapatinib-induced IL-6 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.