ArticleNucleic acids research2014
Engineered reversal of drug resistance in cancer cells--metastases suppressor factors as change agents.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- NM23/NDPK proteins in transcription regulatory functions and chromatin modulation: emerging trends.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Epigenetic suppression of human telomerase (The Journal of biological chemistry · 2017Article
- The effect of Nullomer-derived peptides 9R, 9S1R and 124R on the NCI-60 panel and normal cell lines.BMC cancer · 2017Article
- DNA damage-induced ephrin-B2 reverse signaling promotes chemoresistance and drives EMT in colorectal carcinoma harboring mutant p53.Cell death and differentiation · 2016Article
- The human ARF tumor suppressor senses blastema activity and suppresses epimorphic tissue regeneration.eLife · 2015Article
- Escher: A Web Application for Building, Sharing, and Embedding Data-Rich Visualizations of Biological Pathways.PLoS computational biology · 2015Article
- Inhibition of telomerase activity by NME2: impact on metastasis suppression?Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Building molecular correlates of drug resistance in cancer and exploiting them for therapeutic intervention remains a pressing clinical need. To identify factors that impact drug resistance herein we built a model that couples inherent cell-based response toward drugs with transcriptomes of resistant/sensitive cells. To test this model, we focused on a group of genes called metastasis suppressor genes (MSGs) that influence aggressiveness and metastatic potential of cancers. Interestingly, modeling of 84 000 drug response transcriptome combinations predicted multiple MSGs to be associated with resistance of different cell types and drugs. As a case study, on inducing MSG levels in a drug resistant breast cancer line resistance to anticancer drugs caerulomycin, camptothecin and topotecan decreased by more than 50-60%, in both culture conditions and also in tumors generated in mice, in contrast to control un-induced cells. To our knowledge, this is the first demonstration of engineered reversal of drug resistance in cancer cells based on a model that exploits inherent cellular response profiles.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.