bioRxiv ScienceSearch

bioRxiv · 10.1101/512244

Drug combination sensitivity scoring facilitates the discovery of synergistic and efficacious drug combinations in cancer

Abstract

High-throughput drug sensitivity screening has been utilized for facilitating the discovery of drug combinations in cancer. Many existing studies adopted a dose-response matrix design, aiming for the characterization of drug combination sensitivity and synergy. However, there is lack of consensus on the definition of sensitivity and synergy, leading to the use of different mathematical models that do not necessarily agree with each other. We proposed a cross design to enable a more cost-effective testing of sensitivity and synergy for a drug pair. We developed a drug combination sensitivity score (CSS) to summarize the drug combination dose-response curves. Using a high-throughput drug combination dataset, we showed that the CSS is highly reproducible among the replicates. With machine learning approaches such as Elastic Net, Random Forests and Support Vector Machines, the CSS can also be predicted with high accuracy. Furthermore, we defined a synergy score based on the difference between the drug combination and the single drug dose-response curves. We showed that the CSS-based synergy score is able to detect true synergistic and antagonistic drug combinations. The cross drug combination design coupled with the CSS scoring facilitated the evaluation of drug combination sensitivity and synergy using the same scale, with minimal experimental material that is required. Our approach could be utilized as an efficient pipeline for improving the discovery rate in high-throughput drug combination screening. The R scripts for calculating and predicting CSS are available at https://github.com/amalyutina/CSS.\n\nAuthor summaryBeing a complex disease, cancer is one of the main death causes worldwide. Although new treatment strategies have been achieved with cancers, they still have limited efficacy. Even when there is an initial treatment response, cancer cells can develop drug resistance thus cause disease recurrence. To achieve more effective and safe therapies to treat cancer, patients critically need multi-targeted drug combinations that will kill cancer cells at reduced dosages and thereby avoid side effects that are often associated with the standard treatment. However, the increasing number of possible drug combinations makes a pure experimental approach unfeasible, even with automated drug screening instruments. Therefore, we have proposed a new experimental set up to get the drug combination sensitivity data cost-efficiently and developed a score to quantify the efficiency of the drug combination, called drug combination sensitivity score (CSS). Using public datasets, we have shown that the CSS robustness and its highly predictive nature with an accuracy comparable to the experimental replicates. We have also defined a CSS-based synergy score as a metric of drug interaction and justified its relevance. Thus, we expect the proposed computational techniques to be easily applicable and beneficial in the field of drug combination discovery.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Malyutina, A., Majumder, M. M., Wang, W., Pessia, A., Heckman, C. A., Tang, J.. 2019-01-04. Drug combination sensitivity scoring facilitates the discovery of synergistic and efficacious drug combinations in cancer. https://doi.org/10.1101/512244

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Lipid-ASO therapeutics exhibit differential tissue targeted delivery upon systemic or local CNS administration

Antisense oligonucleotides (ASOs) are a powerful therapeutic modality, but their full potential is hindered by pharmacokinetic properties that affect tissue and cellular delivery. Lipid conjugation is increasingly used to modulate ASO's biodistribution and promote extrahepatic activity, yet lipid dependent effects on in vivo functional delivery, particularly in the central nervous system (CNS), remain less explored. Here, we performed a side by side in vivo comparison of cholesterol, palmitic acid (C16:0), docosanoic acid (C22:0), and eicosapentaenoic acid (C20:5) conjugated to a fully phosphorothioated 3 10 3 LNA gapmer ASO targeting the Malat1 long non coding RNA. Lipid-ASO conjugates were administered systemically or locally in the brain of mice and evaluated for tissue level and cellular level distribution by imaging, qPCR and single-cell RNA sequencing, simultaneously annotating cell origin and global transcriptional changes within the cell. Following systemic administration in mice, lipid conjugation improved overall multi organ efficacy compared to unconjugated ASO, but with pronounced tissue specific differences. Single cell sequencing of liver and heart transcriptomes revealed lipid dependent cellular uptake patterns and transcriptional responses distinct from administration of unconjugated ASO. After intracerebroventricular administration, selected fatty acid conjugates enhanced silencing in deep brain regions such as the striatum, whereas cholesterol conjugation impaired functional delivery despite increased CNS retention. Light-sheet microscopy showed restricted parenchymal penetration of cholesterol ASOs compared with broader but heterogeneous distribution of palmitic acid conjugate. Together, these findings demonstrate that lipid identity critically determines ASO efficacy, productive cellular uptake, and regional CNS engagement, emphasizing the need for context specific lipid design in ASO therapeutic development.

pharmacology and toxicology

Novel Dissymmetric Ionizable Lipid-Assembled Lipid Nanoparticles for Delivery of Ferroptosis-Related siRNA in Diabetic Treatment

Small interfering RNA (siRNA) enables precise post-transcriptional gene silencing for refractory diseases, yet its clinical translation remains limited by the lack of safe and efficient delivery vectors. Inspired by the dissymmetric alkyl chain architecture of natural membrane phospholipids, we designed and synthesized 34 novel ionizable lipids with dissymmetric hydrophobic tails and formulated them into lipid nanoparticles (LNPs). Through systematic physicochemical and biological assessments, we established clear structure-activity relationships and identified two lead LNPs (O14-LNP, H18a-LNP) with superior endosomal escape capacity, enhanced in vivo gene silencing potency, and favorable biosafety relative to the clinical benchmark MC3-LNP. In both streptozotocin-induced and spontaneous db/db type 2 diabetes (T2D) mouse models, lead LNPs delivering ferroptosis-related siRNAs effectively ameliorated glucose and lipid metabolic disorders, restored islet function, and alleviated hepatic steatosis. This study not only lays a theoretical foundation for the rational design of novel ionizable lipids, but also validates the therapeutic potential of siRNA therapy targeting ferroptosis, providing a versatile delivery platform and targeted therapeutic strategy for the treatment of T2D.

pharmacology and toxicology

Levetiracetam inhibits SV2A-synaptotagmin interaction at synapses that lack SV2B

Epilepsy remains a difficult-to-treat neurological disorder prompting the need for new therapies that work via alternate mechanisms. Levetiracetam (LEV) is the first in a series of anti-epilepsy drugs that target presynaptic functioning. LEV binds the synaptic vesicle protein SV2A, and has been shown to decrease neurotransmitter release in hippocampal slices. The molecular basis of LEV action is unknown, however, and direct effects of LEV on SV2A function remain to be determined. SV2A is the most widely expressed paralog of a three-gene family (SV2A, B, C) that is variably co-expressed throughout the CNS. All three SV2s bind the calcium sensor protein synaptotagmin and SV2 plays a crucial role in synaptotagmin stability and trafficking. Here we addressed the action of LEV at the cellular and molecular level asking whether the presence of non-LEV binding SV2 paralogs influences drug action and whether LEV impacts SV2As role in synaptotagmin function. We report that LEV altered short-term synaptic plasticity in isolated neurons from SV2B knockout but not wild-type mice, mimicking the loss of SV2 function. Similarly, LEV reduced SV2A binding to synaptotagmin only in the absence of SV2B. Furthermore, LEV reduced and slowed the internalization of synaptotagmin in neurons cultured from SV2B KO but not WT mice. Taken together, these findings suggest that LEV alters synaptic release probability by disrupting SV2s regulation of synaptotagmin selectively in neurons that express only SV2A. Neurons that meet this requirement include most inhibitory neurons and the granule cells of the dentate gyrus, two classes of neuron implicated in epilepsy.

pharmacology and toxicology