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The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have read the journal's policy and have the following conflicts: The authors are employees of Mirna Therapeutics which develops miRNA-based therapies.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: This work was supported by grants from the National Institutes of Health (1R43CA134071, 1R43CA137939, A.G.B.) and a commercialization grant from the Cancer Prevention and Research Institute of Texas (CPRIT). Received: NovemAccepted: JanuPublished: February 14, 2014Ĭopyright: © 2014 Zhao et al.

PLoS ONE 9(2):Įditor: Gerolama Condorelli, Federico II University of Naples, Italy, Italy The data suggest that a majority of NSCLC and other cancers previously not suited for erlotinib may prove sensitive to the drug when used in combination with a miR-34a-based therapy.Ĭitation: Zhao J, Kelnar K, Bader AG (2014) In-Depth Analysis Shows Synergy between Erlotinib and miR-34a. Maximal synergy was detected at dosages that provide a high level of cancer cell inhibition beyond the one that is induced by the single agents alone and, thus, is of clinical relevance. Synergy was observed across a range of different dose levels and drug ratios, reducing IC 50 dose requirements for erlotinib and miR-34a by up to 46-fold and 13-fold, respectively. Our data show a strong synergistic interaction between erlotinib and miR-34a mimics in all cancer cells tested. Using multiple analytical approaches, drug-induced inhibition of cancer cell proliferation was determined to reveal additive, antagonistic or synergistic effects. The drug combination was also tested in a panel of hepatocellular carcinoma cells (HCC), a cancer type known to be refractory to erlotinib. Here, we investigated the relationship of miR-34a and erlotinib and determined the therapeutic activity of the combination in NSCLC cells with primary and acquired erlotinib resistance. Therapeutic miRNA mimics modeled after endogenous tumor suppressor miRNAs inhibit tumor growth by repressing multiple oncogenes at once and, therefore, may be used to augment drug sensitivity. However, the majority of NSCLC and other cancer types remain resistant. Tyrosine kinase inhibitors directed against epidermal growth factor receptor (EGFR-TKI), such as erlotinib, are effective in a limited fraction of non-small cell lung cancer (NSCLC).

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