ArticleBritish journal of cancer2013
Bay11-7082 inhibits the disintegration of the lymphendothelial barrier triggered by MCF-7 breast cancer spheroids; the role of ICAM-1 and adhesion.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Article
- The Therapeutic Potential of Baicalin and Baicalein in Breast Cancer: A Systematic Review of Mechanisms and Efficacy.Current issues in molecular biology · 2025Review
- Highlight: microfluidic devices for cancer metastasis studies.In vitro models · 2022Article
- Role of Lymphatic Endothelium in Vascular Escape of Engineered Human Breast Microtumors.Cellular and molecular bioengineering · 2022Article
- Multiple approaches to repurposing drugs for neuroblastoma.Bioorganic & medicinal chemistry · 2022Article
- Activity in MCF-7 Estrogen-sensitive Breast Cancer Cells of Capsicodendrin fromAnticancer research · 2021Article
- 15-Lipoxygenase and its metabolites in the pathogenesis of breast cancer: A double-edged sword.Lipids in health and disease · 2021Review
- Nuclear factor-κB inhibitor Bay11-7082 inhibits gastric cancer cell proliferation by inhibiting Gli1 expression.Oncology letters · 2021Article
- Flavonoids Distinctly Stabilize Lymph Endothelial- or Blood Endothelial Disintegration Induced by Colon Cancer Spheroids SW620.Molecules (Basel, Switzerland) · 2020Article
- A 17-gene expression-based prognostic signature associated with the prognosis of patients with breast cancer: A STROBE-compliant study.Medicine · 2020Observational
- Targeting AXL and RAGE to prevent geminin overexpression-induced triple-negative breast cancer metastasis.Scientific reports · 2019Article
- In Vitro Modeling of Mechanics in Cancer Metastasis.ACS biomaterials science & engineering · 2018Review
- Chemical Composition ofFrontiers in pharmacology · 2018Article
- Apigenin and Luteolin Attenuate the Breaching of MDA-MB231 Breast Cancer Spheroids Through the Lymph Endothelial BarrierFrontiers in pharmacology · 2018Article
- Colon cancer cell-derived 12(S)-HETE induces the retraction of cancer-associated fibroblast via MLC2, RHO/ROCK and CaCellular and molecular life sciences : CMLS · 2017Article
- The lymphatic system and pancreatic cancer.Cancer letters · 2016Review
- Cancer cell-derived 12(S)-HETE signals via 12-HETE receptor, RHO, ROCK and MLC2 to induce lymph endothelial barrier breaching.British journal of cancer · 2016Article
- Article
- Targeting the NFκB signaling pathways for breast cancer prevention and therapy.Current medicinal chemistry · 2015Review
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Authors and funding
20 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMany cancers spread through lymphatic routes, and mechanistic insights of tumour intravasation into the lymphatic vasculature and targets for intervention are limited. The major emphasis of research focuses currently on the molecular biology of tumour cells, while still little is known regarding the contribution of lymphatics.
methodsBreast cancer cell spheroids attached to lymphendothelial cell (LEC) monolayers were used to investigate the process of intravasation by measuring the areas of 'circular chemorepellent-induced defects' (CCID), which can be considered as entry gates for bulky tumour intravasation. Aspects of tumour cell intravasation were furthermore studied by adhesion assay, and siRNA-mediated knockdown of intracellular adhesion molecule-1 (ICAM-1). Replacing cancer spheroids with the CCID-triggering compound 12(S)-hydroxyeicosatetraenoic acid (HETE) facilitated western blot analyses of Bay11-7082- and baicalein-treated LECs.
resultsBinding of LECs to MCF-7 spheroids, which is a prerequisite for CCID formation, was mediated by ICAM-1 expression, and this depended on NF-κB and correlated with the expression of the prometastatic factor S100A4. Simultaneous inhibition of NF-κB with Bay11-7082 and of arachidonate lipoxygenase (ALOX)-15 with baicalein prevented CCID formation additively.
conclusionTwo mechanisms contribute to CCID formation: ALOX15 via the generation of 12(S)-HETE by MCF-7 cells, which induces directional migration of LECs, and ICAM-1 in LECs under control of NF-κB, which facilitates adhesion of MCF-7 cells to LECs.
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