ArticleCell cycle (Georgetown, Tex.)2015
Anti-protozoal and anti-bacterial antibiotics that inhibit protein synthesis kill cancer subtypes enriched for stem cell-like properties.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Emetine induces oxidative stress, cell differentiation and NF-κB inhibition, suppressing AML stem/progenitor cells.Cell death discovery · 2024Article
- Eradicating the tumor "seeds": nanomedicines-based therapies against cancer stem cells.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2023Review
- Knock down of TIMP-2 by siRNA and CRISPR/Cas9 mediates diverse cellular reprogramming of metastasis and chemosensitivity in ovarian cancer.Cancer cell international · 2022Article
- Review
- Cytostatic and Cytotoxic Natural Products against Cancer Cell Models.Molecules (Basel, Switzerland) · 2019Article
- Mitostemness.Cell cycle (Georgetown, Tex.) · 2018Review
- A mitochondrial based oncology platform for targeting cancer stem cells (CSCs): MITO-ONC-RX.Cell cycle (Georgetown, Tex.) · 2018Review
- Identification of breast cancer hub genes and analysis of prognostic values using integrated bioinformatics analysis.Cancer biomarkers : section A of Disease markers · 2017Article
- Article
- Emetine induces estrogen receptor alpha degradation and prevents 17β-estradiol-induced breast cancer cell proliferation.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- BRCA1 haploinsufficiency cell-autonomously activates RANKL expression and generates denosumab-responsive breast cancer-initiating cells.Oncotarget · 2017Article
- Article
- Amicoumacin A induces cancer cell death by targeting the eukaryotic ribosome.Scientific reports · 2016Article
- Doxycycline and therapeutic targeting of the DNA damage response in cancer cells: old drug, new purpose.Oncoscience · 2015Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Key players in translational regulation such as ribosomes might represent powerful, but hitherto largely unexplored, targets to eliminate drug-refractory cancer stem cells (CSCs). A recent study by the Lisanti group has documented how puromycin, an old antibiotic derived from Streptomyces alboniger that inhibits ribosomal protein translation, can efficiently suppress CSC states in tumorspheres and monolayer cultures. We have used a closely related approach based on Biolog Phenotype Microarrays (PM), which contain tens of lyophilized antimicrobial drugs, to assess the chemosensitivity profiles of breast cancer cell lines enriched for stem cell-like properties. Antibiotics directly targeting active sites of the ribosome including emetine, puromycin and cycloheximide, inhibitors of ribosome biogenesis such as dactinomycin, ribotoxic stress agents such as daunorubicin, and indirect inhibitors of protein synthesis such as acriflavine, had the largest cytotoxic impact against claudin-low and basal-like breast cancer cells. Thus, biologically aggressive, treatment-resistant breast cancer subtypes enriched for stem cell-like properties exhibit exacerbated chemosensitivities to anti-protozoal and anti-bacterial antibiotics targeting protein synthesis. These results suggest that old/existing microbicides might be repurposed not only as new cancer therapeutics, but also might provide the tools and molecular understanding needed to develop second-generation inhibitors of ribosomal translation to eradicate CSC traits in tumor tissues.
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