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Your search keyword '"Reisenauer, Keighley N."' showing total 2 results
Start Over Author "Reisenauer, Keighley N." Publisher nature publishing group uk
2 results on '"Reisenauer, Keighley N."'

2. Epithelial-mesenchymal transition sensitizes breast cancer cells to cell death via the fungus-derived sesterterpenoid ophiobolin A

Author

Saawan D. Patel, Shuxuan Song, Provas Das, Alec Ingros, Sheridan Mikhail, Haleigh Svatek, Angela Boari, Peter Sheesley, Antonio Evidente, Yongfeng Tao, Alexander Kornienko, Marco Masi, Daniel Romo, Joseph H. Taube, Keighley N. Reisenauer, Reisenauer, Keighley N, Tao, Yongfeng, Das, Prova, Song, Shuxuan, Svatek, Haleigh, Patel, Saawan D, Mikhail, Sheridan, Ingros, Alec, Sheesley, Peter, Masi, Marco, Boari, Angela, Evidente, Antonio, Kornienko, Alexander, Romo, Daniel, and Taube, Joseph

Subjects
ophiobolin A, Programmed cell death, natural product, Cell biology, Epithelial-Mesenchymal Transition, Sesterterpenes, Cancer therapy, medicine.medical_treatment, Science, Breast Neoplasms, Mice, SCID, Article, Cancer stem cell, In vivo, Cell Line, Tumor, medicine, Animals, Humans, Doxorubicin, Epithelial–mesenchymal transition, Cytotoxicity, Drechslera, Cancer, Cell Proliferation, Chemotherapy, Multidisciplinary, Cell Death, Chemistry, Cancer stem cells, Twist-Related Protein 1, Fungi, Nuclear Proteins, Epithelial Cells, medicine.disease, Gene Expression Regulation, Neoplastic, MicroRNAs, Aspergillus, Phenotype, embryonic structures, Cancer research, cytotoxicity, Medicine, Female, medicine.drug
Abstract

The epithelial–mesenchymal transition (EMT) imparts properties of cancer stem-like cells, including resistance to frequently used chemotherapies, necessitating the identification of molecules that induce cell death specifically in stem-like cells with EMT properties. Herein, we demonstrate that breast cancer cells enriched for EMT features are more sensitive to cytotoxicity induced by ophiobolin A (OpA), a sesterterpenoid natural product. Using a model of experimentally induced EMT in human mammary epithelial (HMLE) cells, we show that EMT is both necessary and sufficient for OpA sensitivity. Moreover prolonged, sub-cytotoxic exposure to OpA is sufficient to suppress EMT-imparted CSC features including sphere formation and resistance to doxorubicin. In vivo growth of CSC-rich mammary cell tumors, is suppressed by OpA treatment. These data identify a driver of EMT-driven cytotoxicity with significant potential for use either in combination with standard chemotherapy or for tumors enriched for EMT features.

Published
2021

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