ArticleAnnals of medicine and surgery (2012)2022
Evaluating the effect of Alantolactone on the expression of N-cadherin and Vimentin genes effective in epithelial-mesenchymal transition (EMT) in breast cancer cell line (MDA-MB-231).
Article in Annals of medicine and surgery (2012), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- FAK regulates leptin-induced angiogenesis and vasculogenic mimicry in breast cancer.Medical oncology (Northwood, London, England) · 2026Article
- Isoalantolactone Attenuates LPS-Induced Acute Lung Injury, an Effect Associated with Suppressed MAPK/STAT3 Activation and Epithelial-Mesenchymal Transition.International journal of medical sciences · 2026Article
- Bottom-Up Synthesis and Purification of Extracellular Vesicle Mimetics.Journal of extracellular vesicles · 2025Article
- Alantolactone Inhibits Double Expression Lymphoma via Dual-Targeted Glycogen Synthase Kinase 3 Beta and B-Cell Lymphoma2.Blood and lymphatic cancer : targets and therapy · 2025Article
- Therapeutic Potential of Natural Compounds to Modulate WNT/β-Catenin Signaling in Cancer: Current State of Art and Challenges.International journal of molecular sciences · 2024Review
- From Sea to Science: Coral Aquaculture for Sustainable Anticancer Drug Development.Marine drugs · 2024Article
- Erratum: Evaluating the effect of Alantolactone on the expression of N-cadherin and Vimentin genes effective in epithelial-mesenchymal transition (EMT) in breast cancer cell line (MDA-MB-231): erratum.Annals of medicine and surgery (2012) · 2024Article
- RBCK1 is an endogenous inhibitor for triple negative breast cancer via hippo/YAP axis.Cell communication and signaling : CCS · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveBreast cancer is the second leading cause of death and the most common cancer among women. 10 to 20 percent of breast cancer samples have a negative triple phenotype that is more metastatic and more difficult to diagnose. Tumor invasion to other tissues and the formation of a secondary tumor depend on the epithelial to mesenchymal transition process, and the STAT3 pathway, which is associated with tumor proliferation and invasion and is the target gene for the drug, alantolactone. In this study, the EMT process is evaluated in negative triple-breasted cancer cells treated with alantolactone.
methodsWe used MDA-MB-231 cell line for assessing the survival rate of triple negative breast cancer cells and MTT test for determining alantolactone dose. We used three doses of 0.01 0.1, and 1 μM of alantolactone for evaluating the cell behavior in cancer invasion pathway. Real-time PCR was used to evaluate the expression of Vimentin, and N-cadherin genes. All of the tests were repeated thrice and the data were analyzed using Prism version 7.0.
resultsThe expression of Vimentin and N-cadherin decreased significantly at 1 μM alantolactone compared to the control group, p < 0.05.
conclusionAlantolactone affects the expression of Vimentin and N-cadherin through STAT3 signaling pathway and suppresses EMT process, metastasis and cancer invasion. This component may be used for treatment of patients with breast cancer.
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