ArticleJournal of translational medicine2023
Cantharidin induces apoptosis of human triple negative breast cancer cells through mir-607-mediated downregulation of EGFR.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Analysis of Clinical Trials Using Anti-Tumor Traditional Chinese Medicine Monomers.Drug design, development and therapy · 2024Pooled it
- Cantharidic acid causes mitochondrial dysfunction via the Nrf2/HO-1/GPX4 pathway to inhibit colorectal cancer progression.Histology and histopathology · 2026Article
- Aptamer-Mediated Dual-Loaded Liposomal Nanosystem for Synergistic Therapy in Hepatocellular Carcinoma via mTOR/HIF-1α/VEGF Pathway.International journal of nanomedicine · 2026Article
- Network Pharmacology and Experimental Validation Reveal Aidi Injection Suppresses Prostate Cancer via EGFR Inhibition and STAT3-Mediated Apoptosis.Biological procedures online · 2025Article
- An overview of the research progress on Mylabris: entomology, active ingredients, traditional use, pharmacology, clinical application, pharmacokinetics, toxicity and detoxification strategies.Chinese medicine · 2025Review
- pH-responsive 2D niobium carbide nanosheets for targeted circPUM1 siRNA delivery in ovarian cancer therapy.Materials today. Bio · 2025Article
- Traditional Chinese medicine in the treatment of breast Cancer.Molecular cancer · 2025Review
- Role of the P2X7 receptor in breast cancer progression.Purinergic signalling · 2025Review
- Discovery of novel antimyeloma agents targeting TRIP13 by molecular modeling and bioassay.RSC medicinal chemistry · 2025Article
- Targeting kinases that regulate programmed cell death: a new therapeutic strategy for breast cancer.Journal of translational medicine · 2025Review
- Research progress on the signaling pathway mechanism of terpenoids against breast cancer.Discover oncology · 2025Review
- Cancer patient-derived organoids: Novel models for the study of natural products.International journal of biological sciences · 2025Review
- Mylabris: a review of its biological characteristics, chemical composition, pharmacological, toxicology, pharmacokinetics, and marketed drugs.Frontiers in pharmacology · 2025Review
- Targeting the Inactive Conformation of the Epidermal Growth Factor Receptor Identifies EG31: A Novel Small Molecule Inhibitor Effective Against Normal and 5-Fluorouracil-Resistant Triple Negative Breast Cancer Cells.OncoTargets and therapy · 2025Article
- The study on circRNA profiling uncovers the regulatory function of the hsa_circ_0059665/miR-602 pathway in breast cancer.Scientific reports · 2024Article
- Impact of microRNA variants on PI3K/AKT signaling in triple-negative breast cancer: comprehensive review.Medical oncology (Northwood, London, England) · 2024Review
- Transcriptomic analysis reveals regulation of adipogenesis via long non-coding RNA, alternative splicing, and alternative polyadenylation.Scientific reports · 2024Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple negative breast cancer (TNBC) is a major subtype of breast cancer, with limited therapeutic drugs in clinical. Epidermal growth factor receptor (EGFR) is reported to be overexpressed in various TNBC cells. Cantharidin is an effective ingredient in many clinical traditional Chinese medicine preparations, such as Delisheng injection, Aidi injection, Disodium cantharidinate and vitamin B6 injection. Previous studies showed that cantharidin had satisfactory pharmacological activity on a variety of tumors. In this study, we aimed to study the therapeutic potential of cantharidin for TNBC treatment by targeting EGFR, and expound its novel regulator miR-607.
methodsThe effect of cantharidin on breast cancer in vivo was evaluated by 4T1 mice model. Then the effects of cantharidin on TNBC cells was assessed by the MTT, colony formation, and AnnexinV-PE/7AAD staining. Cantharidin acts on EGFR were verified using the cell membrane chromatography, RT-PCR, Western blotting, MTT, and so on. Mechanistic studies were explored by dual-luciferase report assay, RT-PCR, western blotting, and immunofluorescence staining assay.
resultsCantharidin inhibited TNBC cell growth and induce apoptosis by targeting EGFR. miR-607 was a novel EGFR regulator and exhibited suppressive functions on TNBC cell behaviors. Mechanistic study showed that cantharidin blocked the downstream PI3K/AKT/mTOR and ERK/MAPK signaling pathway.
conclusionOur results revealed that cantharidin may be served as a potential candidate for TNBC treatment by miR-607-mediated downregulation of EGFR.
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