Co-inhibition of mTORC1, HDAC and ESR1α retards the growth of triple-negative breast cancer and suppresses cancer stem cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-08

AUTHORS

Andrew Sulaiman, Sarah McGarry, Ka Mien Lam, Sara El-Sahli, Jason Chambers, Shelby Kaczmarek, Li Li, Christina Addison, Jim Dimitroulakos, Angel Arnaout, Carolyn Nessim, Zemin Yao, Guang Ji, Haiyan Song, Sheng Liu, Ying Xie, Suresh Gadde, Xuguang Li, Lisheng Wang

ABSTRACT

Triple-negative breast cancer (TNBC) is the most refractory subtype of breast cancer. It causes the majority of breast cancer-related deaths, which has been largely associated with the plasticity of tumor cells and persistence of cancer stem cells (CSCs). Conventional chemotherapeutics enrich CSCs and lead to drug resistance and disease relapse. Development of a strategy capable of inhibiting both bulk and CSC populations is an unmet medical need. Inhibitors against estrogen receptor 1, HDACs, or mTOR have been studied in the treatment of TNBC; however, the results are inconsistent. In this work, we found that patient TNBC samples expressed high levels of mTORC1 and HDAC genes in comparison to luminal breast cancer samples. Furthermore, co-inhibition of mTORC1 and HDAC with rapamycin and valproic acid, but neither alone, reproducibly promoted ESR1 expression in TNBC cells. In combination with tamoxifen (inhibiting ESR1), both S6RP phosphorylation and rapamycin-induced 4E-BP1 upregulation in TNBC bulk cells was inhibited. We further showed that fractionated CSCs expressed higher levels of mTORC1 and HDAC than non-CSCs. As a result, co-inhibition of mTORC1, HDAC, and ESR1 was capable of reducing both bulk and CSC subpopulations as well as the conversion of fractionated non-CSC to CSCs in TNBC cells. These observations were partially recapitulated with the cultured tumor fragments from TNBC patients. Furthermore, co-administration of rapamycin, valproic acid, and tamoxifen retarded tumor growth and reduced CD44high/+/CD24low/- CSCs in a human TNBC xenograft model and hampered tumorigenesis after secondary transplantation. Since the drugs tested are commonly used in clinic, this study provides a new therapeutic strategy and a strong rationale for clinical evaluation of these combinations for the treatment of patients with TNBC. More... »

PAGES

815

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41419-018-0811-7

DOI

http://dx.doi.org/10.1038/s41419-018-0811-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1105854198

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30050079


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418 China-Canada Centre of Research for Digestive Diseases, University of Ottawa, 451 Smyth Road, K1H 8M5, Ottawa, ON, Canada
419 Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, 451 Smyth Road, K1H 8M5, Ottawa, ON, Canada
420 Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 725 South Wanping Road, 200032, Shanghai, China
421 Ottawa Institute of Systems Biology, University of Ottawa, 451 Smyth Road, K1H 8M5, Ottawa, ON, Canada
422 Regenerative Medicine Program, Ottawa Hospital Research Institute, K1H 8L6, Ottawa, ON, Canada
423 rdf:type schema:Organization
 




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